Hepatoprotective effects of licochalcone B on carbon tetrachloride-induced liver toxicity in mice

Objective(s): The objective of this study was to investigate the hepatoprotective effect of licochalcone B (LCB) in a mice model of carbon tetrachloride (CCl۴)-induced liver toxicity. Materials and Methods: Hepatotoxicity was induced in mice by a single subcutaneous injection (SC) of CCl۴. The LCB was administered orally once a day for seven days (PO) as pretreatment at three doses of ۱, ۵, and ۲۵ mg/kg/day. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), glutathione disulfide (GSSG), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-۶ (IL-۶), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA. The protein expression degrees of p۳۸ mitogen activated protein kinases (p۳۸) and nuclear factor-k-gene binding (NF-κB) were assayed by western blotting. Results: CCl۴-induced hepatotoxicity was manifested by an increase in the levels of ALT, AST, MDA, IL-۶, CRP, and TNF-ɑ, and a decrease in the SOD level and GSH/GSSG ratio in the serum. The histopathological examination of the liver sections revealed necrosis and inflammatory reactions. Pretreatment with LCB decreased the levels of ALT, AST, MDA, GSSG, IL-۶, CRP, TNF-ɑ, and the protein expression of p۳۸ and NF-κB, increased the level of SOD and GSH, and normalized the hepatic histo-architecture. Conclusion: LCB protected the liver from CCl۴-induced injury. Protection may be due to inhibition of p۳۸ and NFκB signaling, which subsequently reduced inflammation in the liver.

Keywords:

Antioxidant , Anti-inflammatory , Carbon tetrachloride , Hepatotoxicity , Licochalcone B , NF-κB , p۳۸