Anti-inflammatory and hepatoprotective effects of Ganoderma lucidum polysaccharides on carbon tetrachloride-induced hepatocyte damage in common carp (Cyprinus carpio L.)
文献类型: 外文期刊
第一作者: Liu, Ying-Juan
作者: Liu, Ying-Juan;Jia, Rui;Shen, Yu-Jin;Zhao, Cai-Yuan;Yin, Guo-Jun;Du, Jin-Liang;Cao, Li-Ping;Xu, Pao;Yin, Guo-Jun;Du, Jin-Liang;Cao, Li-Ping;Xu, Pao;Yin, Guo-Jun
作者机构:
关键词: Hepatoprotective effects;Immune inflammatory response;Apoptosis;Ganoderma lucidum polysaccharides;CCl4;Liver injury
期刊名称:INTERNATIONAL IMMUNOPHARMACOLOGY ( 影响因子:4.932; 五年影响因子:4.624 )
ISSN: 1567-5769
年卷期: 2015 年 25 卷 1 期
页码:
收录情况: SCI
摘要: The aim of this study was to investigate the anti-inflammatory and hepatoprotective effects of Ganoderma lucidum polysaccharides (GLPS) on carbon tetrachloride (CCl4)-induced hepatocyte damage in common carp (Cyprinus carpio L.). GLPS (0.1, 03, 0.6 mg/ml were added to the primary hepatocytes before (pre-treatment), after (post-treatment) and both before and after (pre- and post-treatment) the incubation of the hepatocytes with CCl4 at the concentration of 8 mM in the culture medium. The supernatants and cells were collected respectively to detect the biochemical indicators. The levels of TNF-alpha, IL-1 beta, caspase-3 and caspase-8 were measured by ELISA, the mRNA expressions of CYP1A and CYP3A were determined by RT-PCR, and western blotting was used to assay the relative protein expressions of c-Rel and p65. Results showed that GLPS significantly improved cell viability and inhibited the elevations of the marker enzymes (GOT, GPT, LDH) and MDA induced by CCl4, and markedly increased the level of SOD. Treatments with GLPS resulted in a significant decrease in the expressions of CYP1A and CYP3A, and significantly down-regulated extrinsic apoptosis and immune inflammatory response. In brief, the present study showed that GLPS can protect hepatocyte injury induced by CCl4 through inhibiting lipid peroxidation, elevating antioxidant enzyme activity and suppressing apoptosis and immune inflammatory response. (C) 2015 Elsevier B.V. All rights reserved.
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