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

作者：Teng, Haifeng^*; Chen, Meng; Zou, Ansheng; Jiang, Haili; Han, Jichun; Sun, Long; Feng, Chao; Liu, Ju

来源：Iranian Journal of Basic Medical Sciences, 2016, 19(8): 910-915.

• Antioxidant
• Anti-inflammatory
• Carbon tetrachloride
• Hepatotoxicity
• Licochalcone B
• NF-kappa B
• P38

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-a (TNF-alpha), 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-kappa B) 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-alpha, 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-alpha, and the protein expression of p38 and NF-kappa B, increased the level of SOD and GSH, and normalized the hepatic histoarchitecture. @@@ Conclusion: LCB protected the liver from CCl4-induced injury. Protection may be due to inhibition of p38 and NF-kappa B signaling, which subsequently reduced inflammation in the liver.

• 出版日期2016-8
• 单位烟台毓璜顶医院; 上海中医药大学; 山东省千佛山医院