| Literature DB >> 32067515 |
Shuang Chen1, Chun-Lei Zhang1, Xiao-Fei Zhou1, Yu Gao1, Hao Chen1, Ben-Dong Fu1, Peng-Fei Yi1, Hai-Qing Shen1.
Abstract
Acute liver injury can be caused by chemicals and can lead to liver failure. We investigated the protective effect of helicid (HEL) on acute liver injury caused by CCl4 in mice. We found that ALT and AST levels as well as hepatic pathological damage in mice treated with CCl4 was increased significantly, while the effects were decreased by HEL treatment. HEL treatment increased the activity of T-SOD, GSH and CAT and reduced the level of MDA in CCl4 treated mice. HEL improved the histopathology of liver caused by CCl4. HEL also reduced TNF-α, IL-1β and IL- 6 activity caused by CCl4. We investigated the phosphorylation of p65 and IκB protein and found that HEL can alleviate liver damage via the NF-κB signaling pathway. Our findings indicate that HEL protects against acute liver injury induced by CCl4. The protective effect of HEL appears to be due to its antioxidative and anti-inflammatory properties through the NF-κB signaling pathway.Entities:
Keywords: anti-inflammatory agent; antioxidative agent; carbon tetrachloride; helicid; liver; mice
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Year: 2020 PMID: 32067515 DOI: 10.1080/10520295.2020.1718210
Source DB: PubMed Journal: Biotech Histochem ISSN: 1052-0295 Impact factor: 1.718