• Mendelian randomization
• acute lung injury
• acute pancreatitis
• clinical efficacy
• dexamethasone
• qingyi granule
• rat

• Drugs, Chinese Herbal/pharmacology
• Drugs, Chinese Herbal/chemistry
• Respiratory Distress Syndrome/drug therapy
• Pancreatitis/drug therapy
• Pancreatitis/metabolism
• Animals
• Rats
• Humans
• Retrospective Studies
• Male
• Rats, Sprague-Dawley
• Dexamethasone/pharmacology
• Dexamethasone/administration & dosage
• Acute Disease
• Female
• Middle Aged

• study was supported by the National Key R&D Program of China
• and the National Natural Science Foundation of China

• NF-κB
• Organ damage
• ROS
• Severe acute pancreatitis
• Zerumbone

• Animals
• Rats
• NF-kappa B
• Reactive Oxygen Species
• Pancreatitis/chemically induced
• Pancreatitis/drug therapy
• Acute Disease

• AlCl3
• JAK-2/STAT-3
• Lactobacillus rhamnosus
• PPAR-γ
• Wnt/β-catenin/GSK-3β
• neurotoxicity
• probiotic
• sesamol

• apoptosis
• autophagy
• pathways
• quercetine
• vincristine

Lagotis brachystachya Maxim, a common herb in Tibetan medicine, is mainly used to treat pneumonia, hepatitis, yellow water disease (gouty arthritis). Since long-term heavy drinking is also a risk factor for gouty arthritis, the present study aimed to evaluate the underlying protective role and mechanism of extracts of Lagotis brachystachya (ELB) in chronic alcoholic liver injury combined with gouty arthritis. The rat chronic alcoholic liver injury combined with gouty arthritis model was established by long-term alcohol consumption and monosodium urate (MSU) injection. The therapeutical action of ELB was then evaluated by biochemical measurement, histopathological examination, ankle swelling assessment, and protein detection. According to biochemical measurements and histopathological evaluation, ELB could alleviate the symptoms of alcoholic liver injury combined with gouty arthritis. In addition, chronic alcohol consumption and MSU activated inflammatory-related signaling such as TLR4/MyD88/NF-κB, NLRP3, and JAK2/STAT3 pathways in the liver and synovial tissues, while ELB significantly inhibited the activation of the inflammatory signaling pathway. In conclusion, ELB is protective in rats with chronic alcoholic liver injury and gouty arthritis, possibly mediated by the inhibition of TLR4/MyD88/NF-κB, NLRP3, and JAK2-STAT3 signaling pathways in both the hepatic and synovial tissues.

• HPLC fingerprint
• cerebral ischemia-reperfusion injury
• mathematical model
• spectrum-effect relationship
• yangyin tongnao granules

Fowl Adenovirus serotype 4 (FAdV-4) infection causes severe inflammatory response leading to hepatitis-hydropericardium syndrome (HHS) in poultry. As an essential functional amino acid of poultry, arginine plays a critical role in anti-inflammatory and anti-oxidative stress.

In this study, the differential expression genes (DEGs) were screened by transcriptomic techniques, and the DEGs in gene networks of inflammatory response-induced by FAdV-4 in broiler’s liver were analyzed by Kyoto encyclopedia of genes and genomes (KEGG) enrichment. The results showed that the cytokines pathway and JAK/STAT pathway were significantly enriched, in which the DEGs levels of IL-6, IL-1β, IFN-α, JAK and STAT were significantly up-regulated after FAdV-4 infection. It was further verified with real-time fluorescence quantitative polymerase chain reaction (Real-time qPCR) and Western blotting (WB) in vitro and in vivo. The findings demonstrated that FAdV-4 induced inflammatory response and activated JAK2/STAT3 pathway. Furthermore, we investigated whether arginine could alleviate the liver inflammation induced by FAdV-4. After treatment with 1.92% arginine level diet to broilers or 300 μg/mL arginine culture medium to LMH cell line with FAdV-4 infection at the same time, we found that the mRNA levels of IL-6, IL-1β, IFN-α and the protein levels of p-JAK2, p-STAT3 were down-regulated, compared with FAdV-4 infection group. Furthermore, we confirmed that the inflammation induced by FAdV-4 was ameliorated by pre-treatment with JAK inhibitor AG490 in LMH cells, and it was further alleviated in LMH cells treatment with AG490 and ARG.

These above results provide new insight that arginine protects hepatocytes against inflammation induced by FAdV-4 through JAK2/STAT3 signaling pathway.

The online version contains supplementary material available at 10.1186/s12917-022-03282-9.

• Arginine
• Broiler
• Fowl adenovirus serotype 4
• Inflammation
• JAK2/STAT3 pathway
• Transcriptome

Baicalin (BA) is a kind of flavonoid that is isolated from Scutellaria baicalensis Georgi, which has been verified to have hepatoprotective effects in some diseases. However, the role of BA in acute hepatic injury induced by arsenic trioxide (ATO) remains unclear. The aim of this study was to investigate the protective action of BA on acute hepatic injury induced by ATO and to probe its possible mechanism. Mice were pretreated with BA (50, 100 mg/kg) by gavage. After 7 h, ATO (7.5 mg/kg) was injected intraperitoneally to induce liver injury. After 7 days of treatment, serum and hepatic specimens were collected and assayed to evaluate the hepatoprotective effect of BA. Pathological sections and the liver function index indicated that ATO caused significant liver injury. The fluorescence of reactive oxygen species and oxidative stress indicators showed that ATO also increased oxidative stress. The inflammatory markers in ATO-induced mice also increased significantly. Staining of the terminal deoxynucleotidyl transferase dUTP nick end labeling and apoptotic factor assay showed that apoptosis increased. However, with BA pretreatment, these changes were significantly weakened. In addition, BA treatment promoted the expression of proteins related to the JAK2/STAT3 signaling pathway. The results suggest that BA can ameliorate acute ATO-induced hepatic injury in mice, which is related to the inhibition of oxidative stress, thereby reducing inflammation and apoptosis. The mechanism of this protection is potentially related to the JAK2/STAT3 signaling pathway.

• JAK2/STAT3
• acute hepatic injury
• apoptosis
• arsenic trioxide
• baicalin
• oxidative stress

• Animals
• Antioxidants/metabolism
• Apoptosis/drug effects
• Arsenic Trioxide
• Chemical and Drug Induced Liver Injury/drug therapy
• Chemical and Drug Induced Liver Injury/metabolism
• Chemical and Drug Induced Liver Injury/pathology
• Flavonoids/pharmacology
• Flavonoids/therapeutic use
• Janus Kinase 2/metabolism
• Liver/drug effects
• Liver/metabolism
• Liver/pathology
• Male
• Mice
• Protective Agents/pharmacology
• Protective Agents/therapeutic use
• Reactive Oxygen Species/metabolism
• STAT3 Transcription Factor/metabolism
• Signal Transduction/drug effects

• The Research Foundation of the Administration of Traditional Chinese Medicine of Hebei Province, China

Acute pancreatitis (AP) is a very common acute disease, and the mortality rate of severe AP (SAP) is between 15% and 35%. The main causes of death are multiple organ dysfunction syndrome and infections. The mortality rate of patients with SAP related to liver failure is as high as 83%, and approximately 5% of the SAP patients have fulminant liver failure. Liver function is closely related to the progression and prognosis of AP. In this review, we aim to elaborate on the clinical manifestations and mechanism of liver injury in patients with AP.

• Acute pancreatitis
• Liver injury
• Liver dysfunction
• Cytokines
• Oxidative stress

• hypoxia
• inflammation
• liver
• oxidative stress
• salidroside

• National Natural Science Foundation of China
• Natural Science Foundation of Shandong Province

• Acute Disease
• Animals
• Anti-Inflammatory Agents/pharmacology
• Antioxidants/metabolism
• Apoptosis/drug effects
• Bile Acids and Salts/blood
• Cholestasis/pathology
• Cinnamates/chemistry
• Cinnamates/pharmacology
• Cytokines/metabolism
• Hepatocytes/drug effects
• Hepatocytes/pathology
• Iridoid Glucosides/chemistry
• Iridoid Glucosides/pharmacology
• Janus Kinase 2/metabolism
• Liver/enzymology
• Liver/pathology
• Male
• Models, Biological
• Pancreatitis/blood
• Pancreatitis/pathology
• Phosphorylation/drug effects
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• Rats, Sprague-Dawley
• STAT3 Transcription Factor/metabolism
• Signal Transduction
• Rats

• SOCS1/JAK2/STAT3 axis
• brain injury
• cytokines
• in vitro
• in vivo
• inflammation
• microglia
• model
• subarachnoid hemorrhage

Acute biliary pancreatitis (ABP) not only causes acute inflammation of the pancreas, but also leads to obstruction or infection of the biliary system. Liver injury is one of the most common complications of ABP. The pathological mechanisms mainly include infection and endotoxin, cholestasis, pancreatic enzyme damage, microcirculatory disorders, and oxidative stress, and the research conclusions are mostly derived from animal experiments. On the basis of routine medical treatment of ABP, active anti-infective treatment and rapid relief of biliary obstruction can promote the recovery of ABP-related liver injury.

• Acute biliary pancreatitis
• Liver injury
• Biliary obstruction
• Biliary tract infection

Acute inflammation is an important component of the pathogenesis of hepatic ischemia/reperfusion injury (HIRI). Magnesium lithospermate B (MLB) has strong neuroprotective and cardioprotective effects. The purpose of this study was to determine whether MLB had underlying protective effects against hepatic I/R injury and to reveal the potential mechanisms related to the hepatoprotective effects. In this study, we first examined the protective effect of MLB on HIRI in mice that underwent 1 h ischemia followed by 6 h reperfusion. MLB pretreatment alleviated the abnormal liver function and hepatocyte damage induced by I/R injury. We found that serum inflammatory cytokines, including IL-6, IL-1β, and TNF-α, were significantly decreased by MLB during hepatic ischemia/reperfusion (I/R) injury, suggesting that MLB may alleviate hepatic I/R injury via inhibiting inflammatory signaling pathways. Second, we investigated the protein level of p-Jak2/Jak2 and p-Stat3/Stat3 using Western blotting and found that MLB could significantly inhibit the activation of the Jak2/Stat3 signaling pathway, which was further verified by AG490 in a mouse model. Finally, the effect of MLB on the Jak2/Stat3 pathway was further assessed in an in vitro model of RAW 264.7 cells; 1 µg/ml LPS induced the secretion of inflammatory mediators, including IL-6, TNF-α, and activation of the Jak2/Stat3 signaling pathway. MLB significantly inhibited the abnormal secretion of inflammatory factors and the activation of the Jak2/Stat3 signaling pathway in RAW264.7 cells. In conclusion, MLB was found for the first time to reduce inflammation induced by hepatic I/R via suppressing the Jak2/Stat3 pathway.

• Jak2/Stat3 signaling pathway
• acute injury
• anti-inflammation
• hepatic ischemia/reperfusion
• magnesium lithospermate B

• 3D4/21 cells
• DNA methyltransferase
• JAK2/STAT3 pathway
• aflatoxin B1
• immunotoxicity

• Aflatoxin B1/toxicity
• Apoptosis/drug effects
• Cell Line
• Cytokines/genetics
• Cytokines/metabolism
• DNA Damage/drug effects
• DNA Methylation/drug effects
• Gene Expression Regulation
• Humans
• Immunotoxins/toxicity
• Janus Kinase 2/genetics
• Janus Kinase 2/metabolism
• Methyltransferases
• Oxidative Stress/drug effects
• STAT3 Transcription Factor/genetics
• STAT3 Transcription Factor/metabolism

Baicalein (BAI), one of the main components of Scutellaria baicalensis Georgi, possesses numerous pharmacological properties, including anti-cancer, anti-oxidative, anti-virus and anti-bacterial activities. The purpose of this study was to evaluate the hepatoprotective effect of baicalein against acetaminophen (APAP)-exposed liver injury in mice, and elucidate the underlying hepatoprotective mechanism. Baicalein pretreatment significantly alleviated the elevation of IL-6, IL-1β and TNF-α in serum and hepatic in a dose-dependent manner. It also dose-dependently reduced the hepatic malondialdehyde (MDA) concentration, as well as the depletion of hepatic superoxide dismutase (SOD), hepatic glutathione (GSH) and hepatic catalase (CAT). Moreover, pretreatment with baicalein significantly ameliorated APAP-exposed liver damage and histological hepatocyte changes. Baicalein also relieved APAP-induced autophagy by regulating AKT/mTOR pathway, LC3B and P62 expression. Furthermore, the hepatoprotective effect of baicalein to APAP-induced liver injury involved in Jak2/Stat3 and MAPK signaling pathway. Taken together, our findings suggested that baicalein exhibits the ability to prevent liver from APAP-induced liver injury and provided an underlying molecular basis for potential applications of baicalein to cure liver injuries.

• acetaminophen
• autophagy
• baicalein
• inflammation
• liver injury