This research is focused on the metabolomics and cytotoxic effects of the anticancer drug erlotinib encapsulated in poly(lactide-co-glycolide) nanoparticles on non-small cell lung cancer (NSCLC) cell lines.

Uniform-sized nanoparticles (0.325 and 0.068 PDI) with mean diameters of 264.5 and 268.4 nm for blank and erlotinib-PLGA nanoparticles (nanodrugs-NDs) were formulated, respectively. The encapsulation efficiency of prepared nanoparticles was found to be 90.1%. 36% of erlotinib was released from PLGA nanoparticles within 24 h, and the maximum sustained release was 43% at 72 h. The metabolomic and cytotoxic effects of ND were evaluated.

The Bax/Bcl-2 ratio was the lowest in the nanodrug group at 72 h, showing increased apoptosis, indicating that the most effective drug formulation is the combined nanoparticle at 72 h. The metabolomic studies revealed changing amino acids, antioxidant molecules, and carbohydrate profiles. The most significant changes were obtained in pathways related to the synthesis of p-glycoprotein, which is the principal protein for drug efflux and causes drug resistance. The lowest levels of amino acids and polyamines like serine, threonine, spermine, and spermidine were obtained at 72 h with erlotinib encapsulated in poly(lactide-co-glycolide) (PLGA) nanoparticles, showing that the drug resistance may in part be overcome with this nanoparticles.

The encapsulation of erlotinib with PLGA showed effects and influenced critical metabolic pathways, especially pointing out the need to lower drug resistance and signifying it's potential use as an effective treatment strategy for NSCLC.

We aimed to explore the role of Apelin-13 in resisting oxidation, inflammation as well as apoptosis and its underlying mechanisms of action using a model of nicotine-induced H9c2 cardiomyocyte injury.

H9c2 cardiomyocytes were randomly divided into control, nicotine, nicotine + Apelin-13, and Apelin-13 groups. Cell counting kit-8 assay was conducted to determine the cell viability. Interleukin (IL)-6, superoxide dismutase, tumor necrosis factor-alpha (TNF-α), glutathione peroxidase (GSH-Px), IL-β, catalase (CAT), IL-8, lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels were examined. A 2',7'-dichlorodihydrofluorescein diacetate assay was conducted to measure the intracellular reactive oxygen species (ROS) level. The morphology of apoptotic cardiomyocytes was observed by 4',6-diamidino-2-phenylindole staining. Western blotting was employed to measure the protein expressions of apoptotic factors B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X (Bax). Apoptosis was quantified using Annexin V/propidium iodide staining.

Exposure of H9c2 cardiomyocytes to 10 μM nicotine significantly reduced cell viability and increased LDH release, oxidative stress (elevated MDA and ROS levels with decreased superoxide dismutase, GSH-Px, and CAT activities), pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IL-8), and apoptotic markers (increased Bax with decreased Bcl-2 expression, along with nuclear condensation) (p<0.05). In contrast, treatment with 2 μM Apelin-13 significantly alleviated these deleterious effects, enhancing cell viability, restoring antioxidant enzyme activities, reducing oxidative and inflammatory responses, and inhibiting apoptosis (p<0.05).

Nicotine induction increases the oxidative stress and apoptotic capacity of H9c2 cardiomyocytes, but Apelin-13 protects H9c2 cardiomyocytes against nicotine-induced apoptosis and oxidative stress.

Background/Objectives: In 2022, approximately 2.3 million women were diagnosed with breast cancer worldwide, resulting in 670,000 deaths, which accounted for 6.9% of all cancer-related deaths. In the United States, 1 in 8 women will be diagnosed with breast cancer during their lifetime. It was estimated that 2024 would identify about 310,720 women and 2800 men diagnosed with invasive breast cancer. The future global burden of breast cancer is projected to rise to over 3 million new cases and 1 million deaths by 2040. Approximately 20% of breast cancer diagnoses are triple-negative breast cancer (TNBC), a type of cancer that lacks receptors for estrogen (ER-negative), progesterone (PR-negative), and human epidermal growth factor receptor 2 (HER2/neu-negative). Consequently, TNBC does not respond to hormonal or targeted therapies, making it challenging to treat due to its rapid growth, metastasis, and high recurrence rate within the first three years of therapy. Alternative chemotherapies are needed to address this problem. A pharmacological dose of vitamin C (high-dose VC) has been identified as a potential treatment for some cancer cells. The present study aimed to evaluate whether VC has a therapeutic effect on TNBC, using MDA-MB-231 cells as the model. Additionally, VC's effects were trialed on other cancer cells such as MCF7 and on non-cancerous kidney HEK 293 and lung CCL205 cells. Methods: The MTT assay, Hoechst 33342 staining, nuclear-ID red/green staining, Rhodamine 123 staining, and Western blot analysis were employed to test the hypothesis that a pharmacological dose of VC can kill TNBC cells. Results: The upregulation of Apaf-1 and caspases -7, -8, and -9, the inhibition of matrix metalloproteinases (MMP-2 and MMP-9), a reduction in cell cycle protein expression, and the enhancement of tumor suppressor proteins such as p53 and p21 indicate that a pharmacological dose of VC has promising anti-cancer properties in the treatment of breast cancers. Conclusions: Pharmacological dose of VC exerts significant anti-cancer effects in MDA-MB-231 cells by promoting apoptosis, inhibiting metastasis, disrupting cell cycle progression, and enhancing tumor suppressor activity.

The current study demonstrates the biogenic synthesis of silver nanoparticles using the pneumatophores of Acanthus ilicifolius (AiP-AgNPs), which is cost-effective and biocompatible. A. ilicifolius possesses remarkable features to endure the harshest conditions for its entire life cycle and generates secondary metabolites for its sustainability in hostile mangrove ecosystems. The presence of a prominent UV-visible absorption band at 420 nm supported the distinct color change inference for the synthesized AiP-AgNPs. The size of the synthesized AiP-AgNPs was determined to be ∼15 nm through field emission-scanning electron microscopy (FE-SEM), transmission electron microscopy (cryo-TEM), and atomic force microscopy (AFM). The presence of secondary metabolites such as 2-bromo-1,1-dichloroethene, hemin and N-(sulfanylacetyl)-l-seryl-l-argininamide was indicated by prominent peaks in liquid chromatography, suggesting their probable roles in the synthesis of AgNPs. The synthesized AiP-AgNPs demonstrated a distinct zone of inhibition against Pseudomonas aeruginosa (15.33 mm), Vibrio cholerae (9.83 mm), and Bacillus subtilis (12 mm). They also exhibited concentration-dependent antioxidant activity in DPPH, nitric oxide, and hydrogen peroxide scavenging assays. The anticancer potential of the synthesized AiP-AgNPs against HepG2 hepatocarcinoma cells determined through MTT colorimetric assay and flow cytometry revealed their dose-dependent cytotoxicity with the occurrence of the sub-G0 phase (25.6%). Subsequent analysis using fluorescence microscopy, DNA damage, comet assay, and migration assay indicated that AiP-AgNPs hold significant potential and the ability to serve as a therapeutic candidate to pave the way for further in-depth investigations for pre-clinical and clinical research purposes.

The plant kingdom serves as a valuable resource for cancer drug development. This study explored the antitumor activity of different sub-fractions (hexane, dichloromethane and methanol) of U. gallii (gorse) methanol extract in glioblastoma (U-87MG and U-373MG) and neuroblastoma (SH-SY5Y) cell lines, along with their phytochemical profiles. Cytotoxicity was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays, and cell cycle arrest and apoptosis were assessed through flow cytometry and by measuring reactive oxygen species (ROS) and protein expression levels. D7 and D8 dichloromethane sub-fractions significantly reduced cell viability, triggered early apoptosis in SH-SY5Y and U-87MG cells and specifically increased ROS levels in U-87MG cells. Western blot analyses showed that D7 increased p53, caspase-3, caspase-8 and γH2AX expression in SH-SY5Y and U-87MG cells, while D8 specifically elevated p53 in SH-SY5Y cells and caspase-3 in both cell lines. In U-373 cells, D7 and D8 markedly reduced cell viability, with D8 inducing necrosis. Morphological changes indicative of apoptosis were also observed in all cell lines. Bioinformatic analysis of UHPLC-MS and GC-MS data tentatively identified 20 metabolites in D7 and 15 in D8, primarily flavonoids. HPLC-DAD confirmed isoprunetin and genistein as the most abundant in D7 and D8, respectively, both isolated and identified by NMR spectroscopy. Most of the flavonoids identified have been reported as antitumor agents, suggesting that these compounds may be responsible for the observed pharmacological activity.

Frankincense has demonstrated promising in vitro anticancer activity. However, its conventional delivery methods face significant challenges due to limited oral bioavailability. To address these limitations, this study focuses on developing optimized nanoemulsions (NEs) of Frankincense oil (FO) to enhance its therapeutic efficacy.

Frankincense resins were extracted and characterized using gas chromatography-mass spectrometry (GC-MS) and liquid chromatography-mass spectrometry (LC-MS), identifying key metabolites including isopinocarveol, α-thujene, p-cymene, carvone, germacrene A, and various methyl esters. FO-based nanoemulsions (FO-NEs) were prepared and optimized using a 3-factor, 3-level Box-Behnken Design (BBD), with 10% FO (v/v), 40% surfactant (cremophor EL), and co-surfactant (Transcutol P). The optimized FO-NEs were evaluated for particle size, polydispersity index (PDI), zeta potential, and morphology using scanning electron microscopy (SEM) and atomic force microscopy (AFM). Cytotoxicity, wound healing, mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) assays were performed against breast cancer (MDA-MB-231, MDA-MB-231-TR) and lung cancer (A549, A549-TR, H1299) cell lines.

The optimized FO-NEs exhibited an average particle size of 65.1 ± 4.21 nm, a PDI of 0.258 ± 0.04, and a zeta potential of -22.3 ± 1.2 mV. SEM and AFM confirmed the spherical morphology of the FO-NEs. In vitro cytotoxicity studies revealed enhanced anticancer activity of FO-NEs (IC50 = 13.2 μg/mL) compared to free FO (IC50 = 22.5 μg/mL) against resistant breast cancer MDA-MB-231-TR cells. FO-NEs significantly improved cancer cell internalization, disrupted mitochondrial membrane potential, and increased ROS generation, leading to enhanced cytotoxic effects.

The results demonstrate that nanoemulsion-based delivery significantly enhances the bioactivity and cellular uptake of frankincense oil compared to its free form. FO-NEs exhibit potent anticancer activity, particularly against drug-resistant cancer cell lines, suggesting their potential as a viable strategy for improving the therapeutic efficacy of frankincense in cancer treatment.

Cancer is a multifaceted disease characterised by uncontrolled cellular proliferation and metastasis, resulting in significant global mortality. Current therapeutic strategies, including surgery, chemotherapy, and radiation therapy, face challenges such as systemic toxicity and tumour resistance. Recent advancements have shifted towards targeted therapies that act selectively on molecular structures within cancer cells, reducing off-target effects. Mitochondria have emerged as pivotal targets in this approach, given their roles in metabolic reprogramming, retrograde signalling, and oxidative stress, all of which drive the malignant phenotype. Targeting mitochondria offers a promising strategy to address these mechanisms at their origin. Synthetic derivatives of natural compounds hold particular promise in mitochondrial-targeted therapies. Innovations in drug design, including the use of conjugates and nanotechnology, focus on optimizing these compounds for mitochondrial specificity. Such advancements enhance therapeutic efficacy while minimizing systemic toxicity, presenting a significant step forward in modern anticancer strategies.

Patients with high-grade serous carcinoma of tubo-ovarian origin (HGSC) often experience significant side effects related to their disease and treatments, such as pain, discomfort, nausea, and vomiting. Over the last two decades, the use of cannabinoids (CBD) to manage pain and anxiety has become more mainstream. However, there is limited data on how CBD interacts with HGSC tumor cells or whether CBD impacts the effect of chemotherapy. Prior preclinical data has suggested the antitumor benefits of cannabinoids; however, the mechanism and data in ovarian cancer are limited. The objectives of this proposed research are to define the endocannabinoid system milieu in ovarian cancer, determine if CBD influences the growth of ovarian cancer cells, measure the cell viability when cannabinoids such as CBD are combined with standard-of-care therapies, and identify potential molecular pathways in which cannabinoids have a therapeutic effect. We conducted publicly available database searches, in vitro proliferation and apoptotic assays, functional protein signaling via reverse phase protein array analysis of CBD-treated cells using 2D cultured cells, and immunohistological analysis of ex vivo cultured patient-derived tumor slices treated with CBD. Our data suggests that CBD is unlikely to affect the growth of cancer cells at physiologic doses but promotes apoptosis and can have growth inhibitory effects at higher concentrations. The inhibitory effects seen at high dose concentrations are likely from the upregulation of apoptotic pathways and inhibition of oncogenic pathways. Overall, physiologic CBD levels have minimal impact on cancer cell growth or chemotherapy efficacy.

The yellow catfish is an economically significant freshwater fish with increasing importance in aquaculture. However, the low temperature environments prevalent in certain regions pose challenges to its growth, development, and overall health. This study aimed to explore the impact of dietary arginine (Arg) addition on the growth, digestive capacity, and intestinal antioxidant response in fish under low temperature acclimation (18 °C). Total 720 fish were randomly distributed into six groups, each containing 120 fish. Over the course of eight weeks, each group was fed with diets about varying Arg concentrations (1.79-3.26 g/kg). The results indicated that Arg supplementation resulted in an increase in specific growth rate (SGR), feed intake (FI), feed efficiency (FE), as well as pancreatic enzyme activities in both pancreas and intestine. Conversely, malondialdehyde (MDA) and protein carbonyl (PC) contents initially decreased but increased with higher Arg concentrations. Glutathione peroxidase 1a (GPX1a) showed a positive correlation with nuclear factor-erythroid 2-related factor-2 (Nrf2), showing its role in antioxidative capacity. Furthermore, this study revealed that Arg significantly enhanced the activities of anti-superoxide anion, anti-hydroxyl radical, and anti-oxidative enzymes, along with the relative mRNA abundance of Copper-Zinc superoxide dismutase (CuZnSOD), catalase, GPX1a, glutamate-cysteine ligase catalytic subunit (GCLC), and Nrf2 in the intestine. It was determined that yellow catfish weighing between 61.0 g and 89.0 g require an intake of 26.8 g of Arg per kilogram of diet based on polynomial regression analysis of specific growth rate (SGR), which is equivalent to 37.0 g of dietary protein, under sub-low temperature conditions of 18 °C.

This study investigated the potential of a newly synthesized histone deacetylase (HDAC) inhibitor, MHY446, in inducing cell death in HCT116 colorectal cancer cells and compared its activity with that of suberoylanilide hydroxamic acid (SAHA), a well-known HDAC inhibitor. The results showed that MHY446 increased the acetylation of histones H3 and H4 and decreased the expression and activity of HDAC proteins in HCT116 cells. Additionally, MHY446 was confirmed to bind more strongly to HDAC1 than HDAC2 and inhibit its activity. In vivo experiments using nude mice revealed that MHY446 was as effective as SAHA in inhibiting HCT116 cell-grafted tumor growth. This study also evaluated the biological effects of MHY446 on cell survival and death pathways. The reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) confirmed that ROS play a role in MHY446-induced cell death by reducing poly(ADP-ribose) polymerase cleavage. MHY446 also induced cell death via endoplasmic reticulum (ER) stress by increasing the expression of ER stress-related proteins. NAC treatment decreased the expression of ER stress-related proteins, indicating that ROS mediate ER stress as an upstream signaling pathway and induce cell death. While MHY446 did not exhibit superior HDAC inhibition efficacy compared to SAHA, it is anticipated to provide innovative insights into the future development of therapeutic agents for human CRC by offering novel chemical structure-activity relationship-related information.

Externalized phosphatidylserine (PS) is a phospholipid and a selective marker of the tumor microenvironment (TME). It is exposed on the outer leaflet of the plasma membrane of tumor-associated endothelial cells, apoptotic tumor cells, and some viable tumor cells, where it functions in part to suppress immune responses by binding to PS receptors expressed on tumor-infiltrating myeloid cells. PS has been targeted with antibodies, such as bavituximab, that bind the phospholipid via a cofactor, β2-glycoprotein 1 (β2GP1); these antibodies showed excellent specificity for tumor vasculature and induce an immune stimulatory environment. We have advanced this concept by developing the next generation of PS targeting agent, a fusion protein (betabody) constructed by linking PS-binding domain V of β2GP1 to the Fc of an IgG2a. Betabodies bind to externalized PS with high affinity (∼1 nM), without the requirement of a co-factor and localize robustly to the TME. We demonstrate that betabodies are a direct PS-targeting agent that has the potential to be used as anti-tumor therapy, drug delivery vehicles, and tools for imaging the TME.

Despite breakthrough therapeutics in breast cancer, it is one of the main causes of mortality among women worldwide. Thus, drug therapies for treating breast cancer have recently been developed by scientists. Metformin and sorafenib are well-known therapeutics in breast cancer. In the present study, we combined sorafenib and PCL-sorafenib with metformin to improve drug absorption and promote therapeutic efficiency. The MCF-7 cells were treated with metformin, sorafenib, or PCL-sorafenib. The growth inhibitory effect of these drugs and cell viability were assessed using MTT and flow cytometry assays, respectively. The expression of targeted genes involved in cell proliferation, signaling, and the cell cycle was measured by real-time PCR. The results showed that MCF-7 cells treated with metformin/sorafenib and PCL-sorafenib/metformin co-treatment contributed to 50% viability compared to the untreated group. Moreover, PI and Annexin V staining tests showed that the cell viability for metformin/sorafenib and PCL-sorafenib/metformin was 38% and 17%, respectively. Furthermore, sorafenib/metformin and PCL-sorafenib/metformin lead to p53 gene expression increase by which they can increase ROS, thereby decreasing GPX4 gene expression. In addition, they affected the expression of BCL2 and BAX genes and altered the cell cycle. Together, the combination of PCL-sorafenib/metformin and sorafenib/metformin increased sorafenib absorption at lower doses and also led to apoptosis and oxidative stress increases in MCF-7 cells.

Hereditary cancer is estimated to account for up to 10% of the worldwide cancer burden; 5% of all thyroid cancers are thought to be genetic. Inheritance of a deleterious mutation in genes associated with a high lifetime risk of developing cancer. Cancer-predisposing genes can promote the initiation and progression of thyroid cancer by enhancing the activation of major signaling pathways through oxidative stress mechanisms.

Identification of the possible link between familial susceptibility to cancer and the level of oxidative stress in thyroid cancer patients.

Patients with thyroid cancer (with and without genetic predisposition) were investigated. Study participants were treated in Limited Liability Company (LLC) "Oncology Scientific Research Center" (Tbilisi, Georgia). The study group was collected between 2020 and 2021. In patients' blood, the thyroid hormones content (free Triiodothyronine (fFT3), free Thyroxine (fFT4), bound Triiodothyronine (FT3), bound Thyroxine (FT4), Thyroid-stimulating hormone (TSH)), and oxidative stress intensity (total activity of non-enzymatic antioxidant system (TAA) and the lipid peroxidation product, malondialdehyde (MDA), content) were investigated.

The difference in free and bound forms of T3 and T4 levels in the blood serum between patients with thyroid cancer (Group 2 and Group 3) and the control group (Group 1) was not statistically significant (F1,2=0.5, p1,2=0.8, F1,3=2.31, p1,3=0.16). In patients with thyroid cancer the TSH level significantly increased compared to the control group (Group 1) (TSH (mean ± Std error): Group 1- 1.21 ± 0.12, Group 2-2.45 ± 0.11 (F1,2=107, p1,2<0.001), Group 3-2.47 ± 0.17 (F1,3=150, p1,3<0.001)) and the MDA levels increased by 4-5 fold. In patients with thyroid cancer from families with cancer aggregation(Group 2), the level of TAA statistically significantly decreased (F1 - 2=200; p1 - 2<0.001), in patients without genetic predisposition to cancer(Group 3), the level of TAA did not change compared to the control (F1 - 3= 2.13; p1 - 3=0.15), CONCLUSIONS: Oxidative stress plays a critical role in tumorigenesis, and antioxidant/oxidant imbalance may contribute to the malignant transformation of normal tissue. In patients with familial susceptibility to cancer mutations of several genes, which are involved in the regulation of oxidative metabolism, may contribute to the disruption of the redox balance, increase the level of oxidative stress, and contribute to the development of thyroid cancer.

Oxidative stress is a widespread causative agent of disease. Together with its general relevance for biomedicine, such a dynamic is recognizably detrimental to space exploration. Among other solutions, cerium oxide nanoparticles (or nanoceria, NC) display a long-lasting, self-renewable antioxidant activity. In a previous experiment, we evaluated oxidative imbalance in rat myoblasts in space, aboard the International Space Station, and unveiled possible protective effects from NC through RNA sequencing. Here, we focus on the myoblast response to NC on land by means of proteomics, defining a list of proteins that putatively react to NC and confirming nucleosomes/histones as likely mediators of its molecular action. The proteomics data set we present here and its counterpart from the space study share four factors. These are coherently either up- (Hist1h4b) or down-regulated (Gnl3, Mtdh, Trip12) upon NC exposure.

Glioblastoma multiforme (GBM) is a highly aggressive brain cancer with a poor prognosis despite current treatments. This is partially attributed to the immunosuppressive environment facilitated by tumor-associated macrophages, which predominantly underlie the tumor-promoting M2 phenotype. This study investigated the potential of hyperbaric oxygen (HBO) therapy, traditionally used to treat conditions such as decompression sickness, in modulating the macrophage phenotype toward the tumoricidal M1 state and disrupting the supportive tumor microenvironment. HBO has direct antiproliferative effects on tumor cells and reduces hypoxia, which may impair angiogenesis and tumor growth. This offers a novel approach to GBM treatment by targeting the role of the immune system within the tumor microenvironment. The effects of HBO on macrophage polarization and GBM cell viability and apoptosis were evaluated in this study. We detected that HBO promoted M1 macrophage cytokine expression while decreasing GBM cell viability and increasing apoptosis using GBM cell lines and THP-1-derived macrophage-conditioned media. These findings suggest that HBO therapy can shift macrophage polarization toward a tumoricidal M1 state. This can improve GBM cell survival and offers a potential therapeutic strategy. In conclusion, HBO can shift macrophages from a tumor-promoting M2 phenotype to a tumoricidal M1 phenotype in GBM. This can facilitate apoptosis and, in turn, improve treatment outcomes.

Scientists are seeking to find an effective treatment for tumors that has no side effects. N-Acetyl-l-cysteine (NAC) is a thiol compound extracted from garlic. Current study explores the potential of NAC-loaded niosomes (NAC-NIO) for tumor treatment in mice. NAC-loaded niosomes' efficiency, morphology, UV absorption, size distribution, zeta potential, release, and FTIR analysis were evaluated. For vivo study, 25 male BALB/c mice were divided to five groups: gp1 negative control (receive saline), gp2 positive control (tumor group), gp3 treated with NAC, gp4 treated with NAC-NIO at the same time of tumor injection, and gp5 treated with NAC-NIO after tumor growth (day 14). The impact of NAC-NIO on the tumor treatment was evaluated by measuring tumor size progress, comet assay, oxidative stress parameters (GSH, nitric oxide, MDA), western blot analysis, and histopathological investigation of tissues. NAC-NIO showed 72 ± 3% encapsulation efficiency and zeta potential - 5.95 mV with spherical shape. It was found that oral administration of NAC-NIO in a dose of 50 mg/kg provided significant protection against tumor cells. Our formulation decreases DNA injury significantly (P < 0.05). It was noticed that NAC-NIO can increase oxidative stress levels in tumor tissue. On the other hand, the caspase 3 and caspase 9 gene expression were upregulated significantly (P < 0.001) in mice administrated NAC-NIO compared with all other groups. Histological studies confirmed the protective effect of NAC-NIO against tumor especially for treatment during tumor growth protocol. The results suggested that oral delivery of NAC-NIO formulation improved antioxidant effect.

The etiology of colon cancer is either genetic in nature or results from inflammatory bowel diseases such as ulcerative colitis and Crohn's disease; nevertheless, dietary habits play a crucial role in the disease. Wheatgrass is a dietary supplement that is rich in vitamins, minerals, and antioxidants which contribute to health promotion in cardiovascular diseases, liver disease, blood diseases, diabetes, and inflammatory bowel diseases, as well as in several types of cancers, such as oral squamous cell cancer, cervical cancer, and breast cancer. In colorectal cancer (CRC), the prospect that wheatgrass possesses anti-inflammatory, antioxidant, and anticancer properties, and its use as an adjunctive therapy, have been minimally investigated and evidence is still limited. In this review, we compiled the available evidence pertaining to wheatgrass and its likely impact on CRC, described the pathways of inflammation in which wheatgrass could possibly play a role, and identified future research needs on the subject.

As an effective alternative choice to traditional mono-therapy, multifunctional nanoplatforms hold great promise for cancer therapy. Based on the strategies of Fenton-like reactions and reactive oxygen species (ROS)-mediated therapy, black phosphorus (BP) nanoplatform BP@Cu2O@L-Arg (BCL) co-assembly of cuprous oxide (Cu2O) and L-Arginine (L-Arg) nanoparticles was developed and evaluated for synergistic cascade breast cancer therapy.

Cu2O particles were generated in situ on the surface of the BP nanosheets, followed by L-Arg incorporation through electrostatic interactions. In vitro ROS/nitric oxide (NO) generation and glutathione (GSH) depletion were evaluated. In vitro and in vivo anti-cancer activity were also assessed. Finally, immune response of BCL under ultrasound was investigated.

Cu2O was incorporated into BP to exhaust the overexpressed intracellular GSH in cancer cells via the Fenton reaction, thereby decreasing ROS consumption. Apart from being used as biocompatible carriers, BP nanoparticles served as sonosensitizers to produce excessive ROS under ultrasound irradiation. The enhanced ROS accumulation accelerated the oxidation of L-Arg, which further promoted NO generation for gas therapy. In vitro experiments revealed the outstanding therapeutic killing effects of BCL under ultrasound via mechanisms involving GSH deletion and excessive ROS and NO generation. In vivo studies have illustrated that the nanocomplex modified the immune response by promoting macrophage and CD8+ cell infiltration and inhibiting MDSC infiltration.

BCL nanoparticles exhibited multifunctional characteristics for GSH depletion-induced ROS/NO generation, making a new multitherapy strategy for cascade breast cancer therapy.

Oxygen pressure plays an integral role in regulating various aspects of cellular biology. Cell metabolism, proliferation, morphology, senescence, metastasis, and angiogenesis are some instances that are affected by different tensions of oxygen. Hyperoxia or high oxygen concentration, enforces the production of reactive oxygen species (ROS) that disturbs physiological homeostasis, and consequently, in the absence of antioxidants, cells and tissues are directed to an undesired fate. On the other side, hypoxia or low oxygen concentration, impacts cell metabolism and fate strongly through inducing changes in the expression level of specific genes. Thus, understanding the precise mechanism and the extent of the implication of oxygen tension and ROS in biological events is crucial to maintaining the desired cell and tissue function for application in regenerative medicine strategies. Herein, a comprehensive literature review has been performed to find out the impacts of oxygen tensions on the various behaviors of cells or tissues.

The "oxygen effect" improves radiation efficacy; thus, tumor cell oxygen concentration is a crucial factor for improving lung cancer treatment. In the current study, we aimed to identify aerobic exercise-induced changes in oxygen concentrations in non-small cell lung cancer (NSCLC) cells. To this end, an NSCLC xenograft mouse model was established using human A549 cells. Animals were subsequently subjected to aerobic exercise and radiation three times per week for 2 weeks. Aerobic exercise was performed at a speed of 8.0 m/m for 30 min, and the tumor was irradiated with 2 Gy of 6 MV X-rays (total radiation dose 12 Gy). Combined aerobic exercise and radiation reduced NSCLC cell growth. In addition, the positive effect of aerobic exercise on radiation efficacy through oxygenation of tumor cells was confirmed based on hypoxia-inducible factor-1 and carbonic anhydrase IX expression. Finally, whole-transcriptome analysis revealed the key factors that induce oxygenation in NSCLC cells when aerobic exercise was combined with radiation. Taken together, these results indicate that aerobic exercise improves the effectiveness of radiation in the treatment of NSCLC. This preclinical study provides a basis for the clinical application of aerobic exercise to patients with NSCLC undergoing radiation therapy.

The active biological phytochemicals, crucial compounds employed in creating hundreds of medications, are derived from valuable and medicinally significant plants. These phytochemicals offer excellent protection from various illnesses, including inflammatory disorders and chronic conditions caused by oxidative stress. A phenolic monoterpenoid known as eugenol (EUG), it is typically found in the essential oils of many plant species from the Myristicaceae, Myrtaceae, Lamiaceae, and Lauraceae families. One of the main ingredients of clove oil (Syzygium aromaticum (L.), Myrtaceae), it has several applications in industry, including flavoring food, pharmaceutics, dentistry, agriculture, and cosmeceuticals. Due to its excellent potential for avoiding many chronic illnesses, it has lately attracted attention. EUG has been classified as a nonmutant, generally acknowledged as a safe (GRAS) chemical by the World Health Organization (WHO). According to the existing research, EUG possesses notable anti-inflammatory, antioxidant, analgesic, antibacterial, antispasmodic, and apoptosis-promoting properties, which have lately gained attention for its ability to control chronic inflammation, oxidative stress, and mitochondrial malfunction and dramatically impact human wellness. The purpose of this review is to evaluate the scientific evidence from the most significant research studies that have been published regarding the protective role and detoxifying effects of EUG against a wide range of toxins, including biological and chemical toxins, as well as different drugs and pesticides that produce a variety of toxicities, throughout view of the possible advantages of EUG.

To alleviate the burden of water contamination, a newly developed form of bioremediation known as mycofiltration can be employed. Mycofiltration is an environment-friendly technology involving the treatment of contaminated water by passing it through a network of saprophytic fungal mycelium. A mycofilter made of Pleurotus ostreatus was used for the removal of iron (III) and imidacloprid from aqueous solutions. Batch mycofiltration, at a dosage of 1 g of mycofilter per 50 mL, was performed on iron (III) solutions of different concentrations (0.99, 10.7, 22.9, and 27.72 mg/L) and pH (3.3, 7 and 11). For column mycofiltration, the mycofilter was packed into pyrex columns (3.3 × 15 cm) to desired bed heights. Iron (III) and imidacloprid solutions of 18.99 mg/L and 234.70 ng/L, respectively, were filtered at a constant flow rate. Thereafter, Helisoma duryi snails were exposed for 96 h to the respective filtrates, and their catalase and acetylcholinesterase activities were assessed. Batch mycofiltration showed iron (III) removal rates as high as 85%. Column mycofiltration showed removal rates of 94 and 31% for iron (III) and imidacloprid, respectively. Catalase activity was significantly reduced (p < 0.05) in the snails exposed to iron (III) or imidacloprid filtrates, compared to the snails exposed to the non-mycofiltered media. A significantly higher acetylcholinesterase activity was induced by iron (III) filtrates in comparison with the non-mycofiltered media (p < 0.05). There were no significant differences in acetylcholinesterase activity (p > 0.05) in the snails exposed to mycofiltered and non-mycofiltered imidacloprid media. Mycofilter characterisation using Fourier Transform Infrared Spectrophotometry revealed significant changes in transmittance intensity in the mycofilters used for the iron (III) vs the ones used for the imidacloprid solutions. Mycofiltration was found to improve water quality although iron (III) was removed more effectively than imidacloprid.

Polydopamine (PDA)-based nanostructures are used for biomedical purposes. A hybrid drug nanocarrier based on a PDA decorated with polyamidoamine (PAMAM) dendrimers G 3.0 (DG3) followed by a connection with glycol (PEG) moieties, folic acid (FA), and drug doxorubicin (DOX) was used for combined chemo- and photothermal therapy (CT-PTT) of liver cancer. Oxidative stress plays a crucial role in the development of cancer, and PDA seems to have the ability to both donate and accept electrons. We investigated oxidative stress in organs by evaluating oxidative stress markers in vivo. In the liver, the level of reduced glutathione (GSH) was lower and the level of Trolox equivalent antioxidant capacity (TEAC) was higher in the group receiving doxorubicin encapsulated in PDA nanoparticles with phototherapy (PDA@DG3@PEG@FA@DOX + PTT) compared to the control group. The concentration of thiobarbituric acid reactive substances (TBARS) in livers, was higher in the group receiving PDA coated with PAMAM dendrimers and functionalized with PEG and FA (PDA@DG3@PEG@FA) than in other groups. Markers in the brain also showed lower levels of GSH in the PDA@DG3@PEG@FA group than in the control group. Markers of oxidative stress indicated changes in the organs of animals receiving PDA nanoparticles with PAMAM dendrimers functionalized with FA in CT-PTT of liver cancer under in vivo conditions. Our work will provide insights into oxidative stress, which can be an indicator of the toxic potential of PDA nanoparticles and provide new strategies to improve existing therapies.

Cancer sonodynamic therapy (SDT) is the therapeutic strategy of a high-frequency ultrasound (US) combined with a special sonosensitizer that becomes cytotoxic upon US exposure. The growing number of newly discovered sonosensitizers and custom US in vitro treatment solutions push the SDT field into a need for systemic studies and reproducible in vitro experimental set-ups. In the current research, we aimed to compare two of the most used and suitable SDT in vitro set-ups-"sealed well" and "transducer in well"-in one systematic study. We assessed US pressure, intensity, and temperature distribution in wells under US irradiation. Treatment efficacy was evaluated for both set-ups towards cancer cell lines of different origins, treated with two promising sonosensitizer candidates-carbon nanoparticle C60 fullerene (C60) and herbal alkaloid berberine. C60 was found to exhibit higher sonotoxicity toward cancer cells than berberine. The higher efficacy of sonodynamic treatment with a "transducer in well" set-up than a "sealed well" set-up underlined its promising application for SDT in vitro studies. The "transducer in well" set-up is recommended for in vitro US treatment investigations based on its US-field homogeneity and pronounced cellular effects. Moreover, SDT with C60 and berberine could be exploited as a promising combinative approach for cancer treatment.

The article reviews the results of the studies of marker parameters (indicators) of various pathways and mechanisms of apoptosis of lymphocytes in donor peripheral blood induced by UV light (240-390 nm) in doses of 151, 1510, and 3020 J/m2. The article analyses the processes of DNA fragmentation, distortion of the structural asymmetry of the cell membranes, changes in the degree of DNA damage (single-strand breaks), transcriptional factor р53, cytochrome с, Fas receptors (CD95), caspase-3, caspase-8, and caspase-9, reactive oxygen species, and calcium ions in UV modified cells. The study determined that programmed cell death of lymphocytes after UV irradiation with 1510 J/m2 involves the р53-dependent pathway of the nuclear mechanism, as well as receptor-mediated caspase mechanism, mitochondrial mechanism, and the mechanism associated with the defects in calcium homeostasis. Cell death is mediated by reactive oxygen and calcium ions. The article suggests a scheme of possible intracellular events resulting in the apoptotic death of lymphocytes after UV irradiation.

The cellular milieu in which malignant growths or cancer stem cells reside is known as the tumour microenvironment (TME). It is the consequence of the interactivity amongst malignant and non-malignant cells and directly affects cancer development and progression. Reactive oxygen species (ROS) are chemically reactive molecules that contain oxygen, they are generated because of numerous endogenous and external factors. Endogenous ROS produced from mitochondria is known to significantly increase intracellular oxidative stress. In addition to playing a key role in several biological processes both in healthy and malignant cells, ROS function as secondary messengers in cell signalling. At low to moderate concentrations, ROS serves as signalling transducers to promote cancer cell motility, invasion, angiogenesis, and treatment resistance. At high concentrations, ROS can induce oxidative stress, leading to DNA damage, lipid peroxidation and protein oxidation. These effects can result in cell death or trigger signalling pathways that lead to apoptosis. The creation of innovative therapies and cancer management techniques has been aided by a thorough understanding of the TME. At present, surgery, chemotherapy, and radiotherapy, occasionally in combination, are the most often used methods for tumour treatment. The current challenge that these therapies face is the lack of spatiotemporal application specifically at the lesion which results in toxic effects on healthy cells associated with off-target drug delivery and undesirably high doses. Nanotechnology can be used to specifically deliver various chemicals via nanocarriers to target tumour cells, thereby increasing the accumulation of ROS-inducing agents at the site of the tumour. Nanoparticles can be engineered to release ROS-inducing agents in a controlled manner to the TME that will in turn react with the ROS to either increase or decrease it, thereby improving antitumour efficiency. Nano-delivery systems such as liposomes, nanocapsules, solid lipid nanoparticles and nanostructured lipid carriers were explored for the up/down-regulation of ROS. This review will discuss the use of nanotechnology in targeting and altering the ROS in the TME.

The remodeled cancer cell metabolism affects the tumor microenvironment and promotes an immunosuppressive state by changing the levels of macro- and micronutrients and by releasing hormones and cytokines that recruit immunosuppressive immune cells. Novel dietary interventions such as amino acid restriction and periodic fasting mimicking diets can prevent or dampen the formation of an immunosuppressive microenvironment by acting systemically on the release of hormones and growth factors, inhibiting the release of proinflammatory cytokines, and remodeling the tumor vasculature and extracellular matrix. Here, we discuss the latest research on the effects of these therapeutic interventions on immunometabolism and tumor immune response and future scenarios pertaining to how dietary interventions could contribute to cancer therapy.

Acute myeloid leukemia is one of the most commonly identified hematological malignancies with poor prognosis. This research was planned to identify the cytotoxic effects of Auraptene on HL60 and U937 cell lines. The cytotoxic effects of Auraptene were measured by AlamarBlue assay (Resazurin) after 24- and 48-h treatments with different doses of Auraptene. The inductive effects of Auraptene on cellular oxidative stress were investigated by determining cellular ROS levels. The cell cycle progression and cell apoptosis were also evaluated by flow cytometry method. Our findings revealed that Auraptene decreased HL60 and U937 cellular proliferation by downregulation of Cyclin D1. Auraptene also induces cellular oxidative stress by upregulation of cellular ROS levels. Auraptene induces cell cycle arrest the early and late phases of apoptosis by upregulation of Bax and p53 proteins. Our data suggest that the anti-tumor function of Auraptene can be mediated by promoting apoptosis and cell cycle arrest and inducing cellular oxidative stress in HL60 and U937 cell lines. These results support that Auraptene may be used as a potent anti-tumor agent against hematologic malignancies in the further studies.

Heterotheca inuloides, traditionally employed in Mexico, has demonstrated anticancer activities. Although it has been proven that the cytotoxic effect is attributed to cadinane-type sesquiterpenes such as 7-hydroxy-3,4-dihydrocadalene, the mechanism of action by which these agents act in tumor lines and their regulation remain unknown. This study was undertaken to investigate for first time the cytotoxic activity and mechanism of action of 7-hydroxy-3,4-dihydrocadalene and two semi-synthetic cadinanes derivatives towards breast cancer cells.

Cell viability and proliferation were assayed by thiazolyl blue tetrazolium bromide (MTT) assay and Trypan blue dye exclusion assay. Cell migration measure was tested by wound-healing assay. Moreover, the reactive oxygen species (ROS) and lipid peroxidation generation were measured by 2',7'-dichlorofluorescein diacetate (DCFH-DA) assay and thiobarbituric acid reactive substance (TBARS) assay, respectively. Furthermore, expression of caspase-3, Bcl-2 and GAPDH were analyzed by western blot.

The results showed that 7-hydroxy-3,4-dihydrocadalene inhibited MCF7 cell viability in a concentration and time dependent manner. The cytotoxic potency of semisynthetic derivatives 7-(phenylcarbamate)-3,4-dihydrocadalene and 7-(phenylcarbamate)-cadalene was remarkably lower. Moreover, in silico studies showed that 7-hydroxy-3,4-dihydrocadalene, and not so the semi-synthetic derivatives, has optimal physical-chemical properties to lead a promising cytotoxic agent. Further examination on the action mechanism of 7-hydroxy-3,4-dihydrocadalene suggested that this natural product exerted cytotoxicity via oxidative stress as evidenced in a significantly increase of intracellular ROS levels and in an induction of lipid peroxidation. Furthermore, the compound increased caspase-3 and caspase-9 activities and slightly inhibited Bcl-2 levels. Interestingly, it also reduced mitochondrial ATP synthesis and induced mitochondrial uncoupling.

Taken together, 7-hydroxy-3,4-dihydrocadalene is a promising cytotoxic compound against breast cancer via oxidative stress-induction.

Herein, regiospecific nucleophilic ring-opening of spiroaziridine oxindoles has been established to afford 3-substituted-thiooxindole derivatives as anticancer agents. Among the new series, compounds 7d and 9c exhibited promising cytotoxic activity toward HCT-116 cells with IC₅₀ values of 6.73 ± 0.36 and 6.64 ± 0.95 µM, respectively. Further, AO/EB, DCFDA, and DAPI staining studies were executed to establish the underlying apoptosis mechanism which displayed significant nuclear and morphological alterations. JC-1 staining and annexin V binding assay inferred the loss of mitochondrial membrane potential in HCT-116 cancer cells. Cell cycle analysis showed the treatment of 9c against HCT-116 cells, arrested the cell cycle in G2-M phase. In addition, tubulin binding assay revealed that compound 9c exhibited tubulin polymerase inhibition with IC₅₀ value of 9.73 ± 0.18 μM. This inhibition of tubulin polymerase was further supported by binding interactions of 9c with tubulin through docking studies on PDB ID: 3E22.

Despite the high antioxidant and penetration ability of pomegranate seed oil (PSO), the in vivo antitumor activity of PSO nano-emulsion has not been well investigated. Therefore, this study was undertaken to estimate the antitumor activity and safety of PSO nano-emulsion in mice bearing Ehrlich solid carcinoma cells. For tumor inoculation, about 2 × 10⁶ viable Ehrlich tumor cells (200 µl) were implanted intramuscularly in the left thigh of hind leg. Once a solid tumor appears on the 10th day of transplantation; the mice were randomly divided into five groups (5 animals/group). Characterization of the PSO nano-emulsion using a Zeta sizer Malvern instrument and transmission electron microscope (TEM) revealed that the PSO nano-droplets were well dispersed with an average particle size of 8.95 nm and a spherical shape. Treatment with PSO nano-emulsions caused a significant reduction in the tumor size and weight, in a dose dependent manner, compared to tumor control group. Marked dose dependent elevations in the DNA damage level together with significant increases in the tumor suppressor p53, Bax and Caspase genes and reductions in the anti-apoptotic Bcl2 gene were also observed in the tumor tissue of mice given PSO nano-emulsions. Histological examination also revealed apoptosis and necrosis of tumor cells and tumor infiltration with inflammatory cells after PSO nano-emulsion treatment. However, high DNA damage was noticed in the liver and kidney tissues of mice given the highest dose of PSO nano-emulsion (400 mg/kg). Therefore, we concluded that PSO nano-emulsion exhibited a potent antitumor activity through induction of DNA breaks that triggers apoptosis of tumor cells but the highest dose caused genotoxicity to liver and kidney tissues, thus it is recommended to use doses lower than 400 mg/kg of PSO nano-emulsion as an alternative drugs for chemotherapy.

Probiotics are considered a natural source for treating many intestinal disorders, which deliver health benefits in different ways. The study aims to evaluate the immunomodulatory gene expression on HT-29 cell line using Bacillus licheniformis MCC 2514 and Bifidobacterium breve NCIM 5671 as a single culture and in combination. Upon inflammation induced by LPS, the combination of bacteria downregulated the pro-inflammatory cytokines IL-1α (13.4), IL-12 (14.6), IL-8 (2.6), and IL-6 (1.9), and in contrast, TNF-α (21.2) folds has upregulated. However, anti-inflammatory genes such as IL-4 (0.6), IL-10 (2.9), TGF-2 (92.2), and TGF-3 (85.8) folds were upregulated. The combination of bacteria against oxidative stress downregulated the pro-inflammatory cytokines such as IL-1α & β, IL-6, IL-8, IL-12, and IL-18, and upregulated the anti-inflammatory cytokines IL-10, IL-4, TGF-2, and TGF-3. On the introduction of Kocuria rhizophila, the pro-inflammatory cytokines were upregulated. On supplementation of B. licheniformis and B. breve, the upregulated pro-inflammatory cytokines were decreased, and anti-inflammatory cytokines such as IL-4 (6.2), IL-10 (23.5), TGF-2 (166), and TGF-3(28.4) folds were increased. However, gene expression of toll-like receptor-2 was found high (26 folds) upon introducing probiotic bacteria. ELISA results of Interferon-γ found that the expression was higher (7.19 ng/mL) on the introduction of both the bacteria in combination. The higher anti-inflammatory activity was observed when potential probiotic bacteria were used in combination compared to a single culture. Overall study indicates that the combination of aerobic B. licheniformis and anaerobic B. breve has an anti-inflammatory activity that can sustain an excellent gastrointestinal environment during pathogen invasion and inflammation.

The present study determines the possible protective role of fig fruit extract with olive oil and date palm fruit extract (FOD) in decreasing the oral subchronic blood and cardiovascular toxicity of SiO₂NPs, Al₂O₃NPs, or ZnONPs. The present study used 80 male Wistar rats (8 groups, n = 10) distributed according to the treatment. The FOD treatments were used at their recommended antioxidant doses. All nanoparticles (NPs) were given orally and daily at doses of 100 mg/kg for 75 days. The oral administration of different NPs alone led to dramatic, oxidative stress, inflammatory markers, blood coagulation, endothelial dysfunction markers, myocardial enzymes, hematological parameters, lipid profile, and histopathological features compared with the control group. The FOD-NP-treated groups recorded significantly ameliorated blood and cardiovascular toxicity hazards compared to the groups administered with the NPs alone. In conclusion, the administration of FOD provides considerable chemopreventive and ameliorative effects against NP toxicity.

Red claw crayfish (Cherax quadricarinatus) is an important freshwater shrimp species worldwide with enormous economic value. Waterless transportation is an inherent feature of red claw crayfish transportation. However, the high mortality of red claw crayfish is a severe problem in the aquaculture of crayfish after waterless transportation. In this study, we investigated the responses of the hepatopancreas from the red claw crayfish undergoing air exposure stress and normal conditions on transcriptome levels. We used Illumina-based RNA sequencing (RNA-Seq) to perform a transcriptome analysis from the hepatopancreas of red claw crayfish challenged by air exposure. An average of 57,148,800 clean reads per library was obtained, and 33,567 unigenes could be predicted and classified according to their homology with matches in the National Center for Biotechnology Information (NCBI) non-redundant protein sequences (Nr), Gene Ontology (GO), a manually annotated and reviewed protein sequence database (Swiss-Prot), protein families (Pfam), Clusters of Orthologous Groups (COG) of proteins, and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. 690 and 3407 differentially expressed genes (DEGs) were identified between the two stress stages of the red claw crayfish. More DEGs were identified in 12 h, indicating that gene expressions were largely changed at 12 h. Some immune-related pathways and genes were identified according to KEGG and GO enrichment analysis. A total of 12 DEGs involved in immune response and trehalose mechanism were verified by quantitative real-time-polymerase chain reaction (qRT-PCR). The results indicated that the red claw crayfish might counteract the stress of air exposure at the transcriptomic level by increasing expression levels of antioxidant-, immune-, and trehalose metabolism-related genes. These transcriptome results from the hepatopancreas provide significant insights into the influence mechanism of air exposure to the trehalose mechanism and immune response in the red claw crayfish.

Cancer cells exhibit higher proliferation rates than normal cells, and as a consequence, a higher nutritional demand for metabolites such as amino acids. Such cells demonstrate high expression of amino acid transporters and are significantly dependent on the external uptake of amino acids. Moreover, some types of cancer cells exhibit oncogenic mutations that render them auxotrophic to certain amino acids. This metabolic difference between tumor and normal cells has been explored for developing anticancer drugs. Enzymes capable of depleting certain amino acids in the bloodstream can be employed to inhibit the proliferation of cancer cells and promote cell death. Certain microbial enzymes, such as l-asparaginase and l-amino acid oxidases, have been studied for this purpose. In this paper, we discuss the role of l-asparaginase, the only enzyme currently used as a chemotherapeutic agent. We also review the studies on a new potential antineoplastic agent, l-lysine α-oxidase, an enzyme of l-amino acid oxidase family.

Curcumin is an active ingredient isolated from Curcuma longa. It has several pharmacological effects, including anticancer, anti-inflammatory, and antioxidant effects. Due to its low bioavailability, chemical structure instability, and easy oxidation, the application of curcumin has been limited. In this study, to overcome these limitations, curcumin-loaded mesoporous silica nanoparticles (Cur-MSN) were prepared, and the anticancerous effect of Cur-MSNs on head and neck cancer cells, HN5, was investigated. Transmission electron microscopy (TEM) revealed rod-shaped mesoporous nanoparticles with average particle size smaller than 100 nm. Higher cytotoxicity of Cur-MSNs was seen in treated cancer cells compared with free curcumin. The expression of Bcl-2 was significantly reduced in the presence of Cur-MSNs compared to the control (untreated HN5 cells) (p < 0.05). A 3.43-fold increase in the Bax/Bcl-2 ratio was seen in Cur-MSNs treated HN5 cells at the IC50. Cur-MSNs increased intracellular reactive oxygen species (ROS) production. Based on these novel results, we suggest that Cur-MSNs offer efficacy for cancer treatment and future studies should further characterize their properties in various experimental cancer models.

The greatest challenge that limits the application of pyro-catalytic materials is the lack of highly frequent thermal cycling due to the enormous heat capacity of ambient environment, resulting in low pyro-catalytic efficiency. Here, we introduce localized plasmonic heat sources to rapidly yet efficiently heat up pyro-catalytic material itself without wasting energy to raise the surrounding temperature, triggering a significantly expedited pyro-catalytic reaction and enabling multiple pyro-catalytic cycling per unit time. In our work, plasmonic metal/pyro-catalyst composite is fabricated by in situ grown gold nanoparticles on three-dimensional structured coral-like BaTiO3 nanoparticles, which achieves a high hydrogen production rate of 133.1 ± 4.4 μmol·g-1·h-1 under pulsed laser irradiation. We also use theoretical analysis to study the effect of plasmonic local heating on pyro-catalysis. The synergy between plasmonic local heating and pyro-catalysis will bring new opportunities in pyro-catalysis for pollutant treatment, clean energy production, and biological applications.

Oroxylum indicum (L.) Kurz, a medicinal plant, shows numerous pharmacological properties which may be attributed to the bioactive compounds produced by O. indicum or due to associated endophytes. In the present study, leaf of O. indicum was evaluated for the presence of associated fungal endophytes, and antioxidant and cytotoxic activities of bioactive compounds produced from them. Using culture-dependent approach, eight fungal endophytes belonging to five different genera were identified. Two endophytes Daldinia eschscholtzii and Ectophoma multirostrata have been reported for the first time from the leaf of O. indicum plant. High-performance thin-layer chromatography (HPTLC) of ethyl acetate (EA) extract of isolated fungal endophytes showed a distinct fingerprinting profile in EA extract of Colletotrichum gloeosporioides. Among identified endophytes, EA extract of C. gloeosporioides showed significant antioxidant activity against DPPH free radical, superoxide anion radical, nitric oxide radical and hydroxyl radical with EC50 values of 22.24±1.302 μg/mL, 67.46±0.576 μg/mL, 80.10±0.706 μg/mL and 61.55±1.360 μg/mL, respectively. EA extract of C. gloeosporioides exhibited potential cytotoxicity against HCT116, HeLa and HepG2 cancer cell lines with IC50 values of 76.59 μg/mL, 176.20 μg/mL and 1750.70 μg/mL, respectively. A comparative HPTLC fingerprinting and the antioxidant activity of C. gloeosporioides associated with two different hosts (leaf of O. indicum and dead twigs of other plant) showed that C. gloeosporioides produces bioactive compounds in a host-dependent manner.

Chensinin-1b and its lipoanalogs demonstrate different anticancer activities against selected cancer cells, and the anticancer activity of PA-C1b is improved up to 3-fold compared with that of the parent peptide chensinin-1b. However, detailing the mechanism of action of these peptides is required to better understand the structure-function relationship. In this study, chensinin-1b and PA-C1b were selected as the representative peptides to investigate the mode of action in cancer cells. The results indicated that the boundary of the cell membrane was broken when the cells were treated with chensinin-1b, while that of cells treated with PA-C1b remained intact based on morphological changes. Apoptosis assays indicated that PA-C1b induced MCF-7 cancer cell apoptosis, while chensinin-1b mainly damaged the cell membrane. MCF-7 cancer cells treated with the peptides induced the loss of mitochondrial membrane potential, and cytochrome c was released from mitochondria, but PA-C1b enhanced ROS generation. Additionally, PA-C1b uptake occurred via an energy-dependent pathway and was inhibited by selected endocytosis inhibitors. Furthermore, treatment of MCF-7 cells with PA-C1b suppressed Bcl-2 mRNA levels and increased Bax mRNA levels, upregulated the expression of the proapoptotic protein Bax and downregulated the expression of the antiapoptotic protein Bcl-2. These results indicate that the anticancer mechanism of AMPs may be considerably affected by only a slight difference in the hydrophobicity of the two peptides; and such a study may facilitate the design of novel peptide-based anticancer agents.

Prostate cancer is the most commonly diagnosed and frequently occurred cancer in the males globally. The current treatment strategies available to treat prostate cancer are not much effective and express various adverse effects. Hence, there is an urgent need to identify novel treatment that can improve patient outcome. From times immemorial, natural products are highly recognized for novel drug development for various diseases including cancer. Cancer cells generally maintain higher basal levels of reactive oxygen species (ROS) when compared to normal cells due to its high metabolic rate. However, initiation of excess intracellular ROS production can not be tolerated by the cancer cells and induce several cell death signals which are in contrast to normal cells. Therefore, small molecules of natural origin that induce ROS can potentially kill cancer cells in specific and provide a better opportunity to develop a novel drug therapy. In this review, we elaborated various classes of medicinal compounds and their mechanism of killing prostate cancer cells through direct or indirect ROS generation. This can generate a novel thought to develop promising drug candidate to treat prostate cancer patients.

The high lipid content of the brain, coupled with its heavy oxygen dependence and relatively weak antioxidant system, makes it highly susceptible to oxidative DNA damage that contributes to neurodegeneration. This study is aimed at identifying specific ROS-responsive miRNAs that modulate the expression and activity of the DNA repair proteins in human astrocytes, which could serve as potential biomarkers and lead to the development of targeted therapeutic strategies for neurological diseases. Oxidative DNA damage was established after treatment of human astrocytes with 10μM sodium dichromate for 16 h. Comet assay analysis indicated a significant increase in oxidized guanine lesions. RT-qPCR and ELISA assays confirmed that sodium dichromate reduced the mRNA and protein expression levels of the human base-excision repair enzyme, 8-deoxyguanosine DNA glycosylase 1 (hOGG1). Small RNAseq data were generated on an Ion Torrent™ system and the differentially expressed miRNAs were identified using Partek Flow® software. The biologically significant miRNAs were selected using miRNet 2.0. Oxidative-stress-induced DNA damage was associated with a significant decrease in miRNA expression: 231 downregulated miRNAs and 2 upregulated miRNAs (p < 0.05; >2-fold). In addition to identifying multiple miRNA-mRNA pairs involved in DNA repair processes, this study uncovered a novel miRNA-mRNA pair interaction: miR-1248:OGG1. Inhibition of miR-1248 via the transfection of its inhibitor restored the expression levels of hOGG1. Therefore, targeting the identified microRNA candidates could ameliorate the nuclear DNA damage caused by the brain's exposure to mutagens, reduce the incidence and improve the treatment of cancer and neurodegenerative disorders.