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 (ccl4)-induced liver toxicity. materials and methods: hepatotoxicity was induced in mice by a single subcutaneous injection (sc) of ccl4. the lcb was administered orally once a day for seven days (po) as pretreatment at three doses of 1, 5, and 25 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-6 (il-6), alanine aminotransferase (alt) and aspartate aminotransferase (ast) were analyzed by elisa. the protein expression degrees of p38 mitogen activated protein kinases (p38) and nuclear factor-k-gene binding (nf-κb) were assayed by western blotting. results: ccl4-induced hepatotoxicity was manifested by an increase in the levels of alt, ast, mda, il-6, 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-6, crp, tnf-ɑ, and the protein expression of p38 and nf-κb, increased the level of sod and gsh, and normalized the hepatic histo-architecture. conclusion: lcb protected the liver from ccl4-induced injury. protection may be due to inhibition of p38 and nfκb signaling, which subsequently reduced inflammation in the liver.