Licochalcone E protects against carbon tetrachloride‑induced liver toxicity by activating peroxisome proliferator-activated receptor gamma
Affiliations: Department of Clinical College of Chinese and Western Medicine, Binzhou Medical University, Yantai, Shandong 264003, P.R. China, Department of Cardiac Surgery, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, Jiangsu 210008, P.R. China
- Published online on: August 17, 2017 https://doi.org/10.3892/mmr.2017.7268
- Pages: 5269-5276
Copyright: © Han et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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The present study aimed to investigate the hepatoprotective role of Licochalcone E (LCE) and its mechanism of action in a mouse model of carbon tetrachloride (CCl4)‑induced liver toxicity. Hepatotoxicity was induced in Kunming mice via an intraperitoneal injection (IP) of CCl4, 10 ml/kg body weight, diluted with corn oil at a 1:500 ratio. LCE was administered once a day for 7 days (IP) as pretreatment at a dose of 5 mg/kg/day. The levels of C‑reactive protein (CRP) and tumor necrosis factor (TNF)‑α were analyzed to determine the inflammation status. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed using ELISA assays. Liver ultrastructure was observed via optical microscopy. The mRNA and protein expression levels of peroxisome proliferator‑activated receptor (PPAR)γ, and nuclear factor (NF)‑κB were assayed using quantitative polymerase chain reaction and western blot analysis, respectively. Pretreatment with LCE decreased levels of ALT, AST, CRP and TNF‑α, and NF‑κB expression in the experimental hepatotoxicity mice model induced by CCl4. In addition, LCE increased the expression of PPARγ and normalized the hepatic histoarchitecture. However, the effects of LCE were reversed by cotreatment with the PPARγ inhibitor GW9662. The present study suggests that LCE may be used for the treatment of hepatotoxicity, and primarily exhibits its protective role through a PPARγ/NF‑κB‑mediated pathway.