Anti-inflammatory and antioxidative properties of helicid protect against CCl4 induced acute liver injury in mice

被引:9
作者
Chen, Shuang [1 ]
Zhang, Chun-Lei [1 ]
Zhou, Xiao-Fei [1 ]
Gao, Yu [1 ]
Chen, Hao [1 ]
Fu, Ben-Dong [1 ]
Yi, Peng-Fei [1 ]
Shen, Hai-Qing [1 ]
机构
[1] Jilin Univ, Coll Vet Med, 5333 Xian Rd, Changchun 130062, Jilin, Peoples R China
关键词
anti-inflammatory agent; antioxidative agent; carbon tetrachloride; helicid; liver; mice; CARBON-TETRACHLORIDE; OXIDATIVE STRESS; KUPFFER CELLS; PANAX-GINSENG; MODEL; MECHANISMS; DAMAGE; ACTIVATION; FIBROSIS;
D O I
10.1080/10520295.2020.1718210
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
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-alpha, IL-1 beta and IL- 6 activity caused by CCl4. We investigated the phosphorylation of p65 and I kappa B protein and found that HEL can alleviate liver damage via the NF-kappa B 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-kappa B signaling pathway.
引用
收藏
页码:483 / 489
页数:7
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