Yang Xiao-Jun, Liu Jing, Ye Lin-Bai, Yang Fan, Ye Li, Gao Jin-Rong, Wu Zheng-Hui
College of Life Sciences, Wuhan University, Wuhan 430072, Hubei Province, China.
World J Gastroenterol. 2006 Mar 7;12(9):1379-85. doi: 10.3748/wjg.v12.i9.1379.
To investigate the possible mechanism of the protective effects of a bioactive fraction,Ganoderma lucidum proteoglycan (GLPG) isolated from Ganoderma lucidum mycelia, against carbon tetrachloride-induced liver injury.
A liver injury model was induced by carbon tetrachloride. Cytotoxicity was measured by MTT 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-alpha were determined following the instructions of SOD kit and TNF radioimmunoassay kit. Liver sections were stained with hematoxylin and eosin (H and E) for histological evaluation and examined under light microscope.
We found that GLPG can alleviate the L-02 liver cells injury induced by carbon tetrachloride (CCl4) 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 CCl4 with or without GLPG pretreatment indicated that GLPG can significantly suppress the toxicity induced by CCl4 in mice liver. We also found that GLPG reduced TNF-alpha level induced by CCl4 in the plasma of mice, whereas increased SOD activity in the rat serum.
GLPG has hepatic protective activity against CCl4-induced injury both in vitro and in vivo. The possible anti-hepatotoxic mechanisms may be related to the suppression of TNF-alpha level and the free radical scavenging activity.
研究从灵芝菌丝体中分离得到的生物活性组分灵芝蛋白聚糖(GLPG)对四氯化碳诱导的肝损伤的保护作用及其可能机制。
采用四氯化碳诱导肝损伤模型。通过MTT法检测细胞毒性。用自动多功能生化分析仪测定丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)的活性,按照超氧化物歧化酶(SOD)试剂盒和肿瘤坏死因子-α(TNF-α)放射免疫分析试剂盒说明书测定SOD和TNF-α水平。肝组织切片用苏木精-伊红(H&E)染色进行组织学评估,并在光学显微镜下检查。
通过检测ALT和AST活性,我们发现GLPG可减轻四氯化碳(CCl4)诱导的L-02肝细胞损伤,且GLPG作用于L-02细胞未显示任何毒性。此外,对经或未经GLPG预处理的CCl4诱导的小鼠肝损伤进行组织学分析表明,GLPG可显著抑制CCl4对小鼠肝脏的毒性作用。我们还发现GLPG可降低CCl4诱导的小鼠血浆中TNF-α水平,同时提高大鼠血清中SOD活性。
GLPG在体外和体内均对CCl4诱导的损伤具有肝保护活性。其可能的抗肝毒性机制可能与抑制TNF-α水平和清除自由基活性有关。