Alveolar echinococcosis (AE) is a chronic zoonotic parasitic disease caused by infection with Echinococcus multilocularis. AE is associated with a high mortality rate and poses a significant threat to human health. The primary treatment for AE is surgical resection of the lesions; however, owing to its long incubation period and insidious disease progression, many patients are diagnosed only after the onset of complications such as liver cirrhosis, jaundice, and portal hypertension, which preclude curative surgical intervention. For patients who are unwilling or unable to undergo surgery, lifelong administration of anti-AE medications is necessary. Benzimidazole compounds, such as albendazole and mebendazole, are the current mainstays of treatment, offering good efficacy. Nevertheless, these medications primarily inhibit parasite proliferation rather than eradicate the infection, and their long-term use can lead to significant drug-related toxic effects. Consequently, there is an urgent need to develop new therapeutic strategies that convey better efficacy and reduce the adverse effects associated with current treatments. Recent advancements in AE therapy include novel synthetic compounds such as antiviral agents, antibiotics, antineoplastic agents, immunosuppressants, and antiangiogenic agents, as well as natural compounds derived from traditional Chinese and Tibetan medicine. These new drugs show promising clinical potential because they interfere with parasitic metabolic pathways and cellular structures. This review aims to discuss recent research on AE drug therapy, including mechanisms of action, dosing regimens, signalling pathways, and therapeutic outcomes, with a goal of providing new insights and directions for the development of anti-AE drugs and summarizing current advancements in AE pharmacotherapy.

Albendazole (ABZ) and atovaquone (ATO) achieve killing efficacy on Echinococcus granulosus (Egs) by inhibiting energy metabolism, but their utilization rate is low. This study aims to analyze the killing efficacy of ABZ-ATO loading nanoparticles (ABZ-ATO NPs) on Egs.

Physicochemical properties of NPs were evaluated by ultraviolet spectroscopy and nanoparticle size potentiometer. In vitro experiments exmianed the efficacy of ATO, ABZ, or ATO-ABZ NPs on protoscolex activity, drug toxicity on liver cell LO2, ROS production, and energy metabolism indexes (lactic dehydrogenase, lactic acid, pyruvic acid, and ATP). In vivo of Egs-infected mouse model exmianed the efficacy of ATO, ABZ, or ATO-ABZ NPs on vesicle growth and organ toxicity.

Drug NPs are characterized by uniform particle size, stability, high drug loading, and - 21.6mV of zeta potential. ABZ or ATO NPs are more potent than free drugs in inhibiting protoscolex activity. The protoscolex-killing effect of ATO-ABZ NPs was stronger than that of free drugs. In vivo Egs-infected mice experiment showed that ATO-ABZ NPs reduced vesicle size and could protect various organs. The results of energy metabolism showed that ATO-ABZ NPs significantly increased the ROS level and pyruvic acid content, and decreased lactate dehydrogenase, lactic acid content, and ATP production in the larvae. In addition, ATO-ABZ NPs promoted a decrease in DHODH protein expression in protoscolexes.

ATO-ABZ NPs exhibits anti-CE in vitro and in vivo, possibly by inhibiting energy production and promoting pyruvic acid aggregation.

Gills monogenean infestation causes significant mortalities in cultured fishes as a result of respiratory manifestation. Medicinal plants are currently being heavily emphasized in aquaculture due to their great nutritional, therapeutic, antimicrobial activities, and financial value.

The current study is designed to assess the effect of garlic (Allium sativum) and onion (Allium cepa) extracts as a water treatment on the hematological profile, innate immunity, and immune cytokines expression besides histopathological features of gills of Nile tilapia (Oreochromis niloticus L.) infected with gills monogenetic trematodes (Dactylogyrus sp.). Firstly, the 96-hour lethal concentration 50 (96 h-LC50) of garlic extract (GE) and onion extract (OE) were estimated to be 0.4 g/ L and 3.54 g/ L for GE and OE, respectively. Moreover, the in-vitro anti-parasitic potential for (GE) was found between 0.02 and 0.18 mg/mL and 0.4 to 1.8 mg/mL for OE. For the therapeutic trial, fish (n = 120; body weight: 40-60 g) were randomly distributed into four groups in triplicates (30 fish/group, 10 fish/replicate) for 3 days. Group1 (G1) was not infected or treated and served as control. G2 was infected with Dactylogyrus spp. and not exposed to any treatment. G3, G4 were infected with Dactylogyrus sp. and treated with 1/10 and 1/5 of 96 h LC50 of OE, respectively. G5, G6 were infected with Dactylogyrus sp. and treated with 1/10 and 1/5 of 96 h LC50 of GE, respectively.

No apparent signs or behaviors were noted in the control group. Dactylogyrus spp. infected group suffered from clinical signs as Pale color and damaged tissue. Dactylogyrus spp. infection induced lowering of the hematological (HB, MCH, MCHC and WBCs), and immunological variables (lysozyme, nitric oxide, serum Anti- protease activities, and complement 3). the expression of cytokine genes IL-ß and TNF-α were modulated and improved by treatment with A. sativum and A. cepa extracts. The obtained histopathological alterations of the gills of fish infected with (Dactylogyrus spp.) were hyperplasia leading to fusion of the gill filament, lifting of epithelial tissue, aneurism and edema. The results indecated that G4 and G5 is more regenarated epithelium in compare with the control group.

A. sativum and A. cepa extracts enhance the blood profile and nonspecific immune parameters, and down-regulated the expression level of (IL-1β and TNF-α).

Considerable efforts have been made by modern aquaculture to mitigate the environmental damages caused by its practices while also attempting to improve the quality of the aquatic organisms by promoting alternatives, such as the use of natural products, like garlic (Allium sativum), and instead of chemical agents. Garlic has multiple properties, including antifungal, antibacterial, antiviral, antitoxic, and anticancer effects. In fish, the antiparasitic activity of garlic is one of the most reported effects in the literature, mainly using immersion baths for aquatic organisms. Using garlic also has an antimicrobial effect on the culture of aquatic organisms. Therefore, this review focuses on the impact of garlic on the health and production of aquatic organisms.

Background: Hepatic ischemia/reperfusion (I/R) injury to the liver is a significant cause of morbidity and mortality following liver surgery, trauma, and hemorrhagic shock. It was reported that allicin, a type of garlic compound, had a protective effect against other hepatic diseases. Allicin's ability to protect against liver injury caused by ischemic reperfusion remains unknown. As a result, we conducted this study to determine allicin's effects and mechanism of action in hepatic I/R injury. Method: The liver I/R injury model was established by clamping the blood supply to the left and middle liver lobes. Three days prior to the hepatic I/R injury, different concentrations of allicin were gavaged. Then, hepatic function, histological changes, apoptosis markers, oxidative stress, and inflammatory cytokines were measured, and the molecular mechanisms were evaluated using western blot. Another separation experiment used IRAK-M knockout mice and peroxisome proliferator-activated receptor-gamma (PPARγ) inhibitor to deduce the molecular mechanisms. Results: Pretreatment with allicin prior to hepatic I/R injury reduced liver damage by inhibiting aminotransferase activity and alleviating liver injury. It significantly decreased cell apoptosis, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) production, and hepatic oxidative stress. Furthermore, this study demonstrated that GW9662 (inhibitor of PPARγ) abrogated allicin's positive effect by inhibiting PPARγ expression while suppressing IRAK-M expression. Thus, the depletion of IRAK-M cannot influence the expression of PPARγ. The down-regulation of PPARγ-IRAK-M disabled the protection of allicin in I/R injury. Conclusion: Allicin protects against hepatic I/R injury via dose-dependent regulation of the PPARγ-IRAK-M-TLR4 signaling pathway, and it may be a potential drug in future clinical treatment.