Licochalcone E protects against carbon tetrachloride‑induced liver toxicity by activating peroxisome proliferator-activated receptor gamma

摘要: The present study aimed to investigate the hepatoprotective role of Licochalcone E (LCE) and its mechanism action in a mouse model carbon tetrachloride (CCl4)-induced liver toxicity. Hepatotoxicity was induced Kunming mice via an intraperitoneal injection (IP) CCl4, 10 ml/kg body weight, diluted with corn oil at 1:500 ratio. LCE administered once day for 7 days as pretreatment dose 5 mg/kg/day. levels C-reactive protein (CRP) tumor necrosis factor (TNF)-α were analyzed determine inflammation status. alanine aminotransferase (ALT) aspartate (AST) using ELISA assays. Liver ultrastructure observed optical microscopy. mRNA expression peroxisome proliferator-activated receptor (PPAR)γ, nuclear (NF)-κB assayed quantitative polymerase chain reaction western blot analysis, respectively. Pretreatment decreased ALT, AST, CRP TNF-α, NF-κB experimental hepatotoxicity by CCl4. In addition, increased PPARγ normalized hepatic histoarchitecture. However, effects reversed cotreatment inhibitor GW9662. suggests that may be used treatment hepatotoxicity, primarily exhibits protective through PPARγ/NF-κB-mediated pathway.