4.7 Article

Anti-inflammatory and hepatoprotective effects of Ganoderma lucidum polysaccharides on carbon tetrachloride-induced hepatocyte damage in common carp (Cyprinus carpio L.)

期刊

INTERNATIONAL IMMUNOPHARMACOLOGY
卷 25, 期 1, 页码 112-120

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2015.01.023

关键词

Hepatoprotective effects; Immune inflammatory response; Apoptosis; Ganoderma lucidum polysaccharides; CCl4; Liver injury

资金

  1. Central Public-Interest Scientific Institution Basal Research Fund [2014A08YQ01]
  2. National Natural Science Foundation of China [31200918, 31202002]
  3. Jiangsu Science and Technology Department [BK2012535]

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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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