摘要
AIM： To investigate the possible mechanism of the protective effects of a bioactive fraction, Ganoderma lucidum proteoglycan （GLPG）isolated from Ganoderma luddum mycelia, against carbon tetrachloride-induced liver injury. METHODS： A liver injury model was induced by carbon tetrachloride. Cytotoxicity was measured by MTY assay. The activities of alanine aminotransferase （ALT） and aspartate aminotransferase （AST） were determined with an automatic multifunction-biochemical analyzer and the levels of superoxide dismutase （SOD） and TNF-α were determined following the instructions of SOD kit and TNF radioimmunoassay kit. Uver sections were stained with hematoxylin and eosin （H＆E） for histological evaluation and examined under light microscope. RESULTS： We found that GLPG can alleviate the L-02 liver cells injury induced by carbon tetrachloride （CCh） through the measurements of ALT and AST activities and the administration of GLPG to L-02 cells did not display any toxicity. Furthermore, histological analysis of mice liver injury induced by CCh with or without GLPG pretreatment indicated that GLPG can significantly suppress the toxicity induced by CCh in mice liver. We also found that GLPG reduced TNF-α level induced by CCh in the plasma of mice, whereas increased SOD activity in the rat serum. CONCLUSION： GLPG has hepatic protective activity against CCl4 induced injury both in vitro and in vivo. The possible antihepatotoxic mechanisms may be related to the suppression of TNF-α level and the free radical scavenging activity.
瞄准：为了调查 protective 的可能的机制，一份简历完成活跃部分， Ganoderma 易懂嗯从 Ganoderma 孤立的 proteoglycan (GLPG ) 易懂嗯 mycelia，对碳导致四氯化物的肝损伤。方法：一个肝损伤模特儿被四氯化碳劝诱。细胞毒性被 MTT 试金测量。丙氨酸 aminotransferase (中高音) 和 aspartate aminotransferase (著名计算机生产厂商) 的活动与一个自动多功能生物化学的分析器和超级氧化物歧化酶(草皮) 的层次是坚定的， TNF-alpha 被决定遵循草皮工具包和 TNF 放射性免疫测定工具包的指令。肝节为组织学的评估与苏木精和曙红(H 和 E ) 被染色并且在光下面检验了显微镜。结果：我们发现 GLPG 能减轻四氯化碳(CCl4 ) 通过中高音和著名计算机生产厂商活动的大小和 GLPG 的管理导致到房间没显示的 L-02 的 L-02 肝细胞损害任何毒性。而且， CCl4 导致与或没有 GLPG 预告的处理的老鼠肝损伤的组织学的分析显示 GLPG 能显著地压制 CCl4 在老鼠肝导致的毒性。我们也发现了减少的 TNF-alpha 水平在老鼠的血浆由 CCl4 导致了的那 GLPG，而增加在老鼠浆液的草皮活动。结论：GLPG 对导致 CCl4 的损害举办肝的保护的活动在试管内和在活体内。可能的反肝毒素的机制可以与清除的 TNF-alpha 水平和自由基的抑制有关是活动。
基金
Supported by a grant from the Institute of Virology, College of Life Sciences, Wuhan University
