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Oxymatrine Induces Liver Injury through JNK Signalling Pathway Mediated by TNF-α In Vivo
Hong Lu1, Li Zhang2, Li-Li Gu1
1College of Pharmaceutical Science, Zhejiang Chinese Medical University, Hangzhou, China.
Abstract:
Oxymatrine (OMT) is a traditional Chinese medicine monomer and has been used for the treatment of chronic viral hepatitis and many other diseases. We aimed to investigate whether OMT could induce hepatotoxicity in mice and explored the preliminary mechanisms of toxic effects. Twenty-four Institute for Cancer Research male mice were randomly divided into four groups: control group, 40, 160 and 320 mg/kg OMT-treated group. OMT was orally administered once daily for 7 days. The OMT-treated group exhibited an improved liver index and increase in serum alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase,augmented liver histological injury, elevated levels of malondialdehyde and tumour necrosis factor alpha (TNF-α) accompanied by the activation of caspase-9/-8/-3, up-regulated expressions of tumour necrosis factor receptor l (TNFR1), TNF receptor-associated structure domain (TRADD) and phosphorylation of stress-activated protein kinase/c-jun N-terminal protein kinases (p-SAPK/JNK). Altogether, these results suggest that OMT at a dose of 320 mg/kg leads to liver damage and is related to the activation of JNK signalling pathway mediated by TNF-α in the liver of mice.
Insights
Oxymatrine (OMT) may cause liver damage in mice, indicated by elevated liver enzymes and histological injury. This hepatotoxicity is linked to the tumor necrosis factor-alpha (TNF-α) pathway activation and stress-activated protein kinase/c-jun N-terminal protein kinases (SAPK/JNK) signaling.
Area of Science:
- Pharmacology
- Toxicology
- Hepatology
Background:
- Oxymatrine (OMT) is a component of traditional Chinese medicine used for chronic viral hepatitis.
- Its potential for inducing liver toxicity requires investigation.
Purpose of the Study:
- To determine if Oxymatrine (OMT) induces hepatotoxicity in mice.
- To explore the preliminary mechanisms underlying OMT-induced liver damage.
Main Methods:
- Male ICR mice were administered OMT daily for 7 days at doses of 40, 160, and 320 mg/kg.
- Liver index, serum enzymes (ALT, AST, ALP), oxidative stress markers (MDA), inflammatory cytokines (TNF-α), and apoptosis-related proteins (caspase-9/-8/-3) were assessed.
- Expression of TNFR1, TRADD, and p-SAPK/JNK was analyzed.
Main Results:
- OMT treatment, particularly at 320 mg/kg, increased liver index and serum liver enzymes.
- Histological analysis revealed augmented liver injury, elevated MDA and TNF-α levels.
- Activation of caspase-9/-8/-3, upregulation of TNFR1, TRADD, and phosphorylation of SAPK/JNK were observed.
Conclusions:
- Oxymatrine (OMT) at 320 mg/kg induces significant liver damage in mice.
- OMT-induced hepatotoxicity is associated with TNF-α-mediated activation of the JNK signaling pathway.
