首页> 外文期刊>World Journal of Gastroenterology >In vitro and in vivo protective effects of proteoglycan isolated from mycelia of Ganoderma lucidum on carbon tetrachloride-induced liver injury.
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In vitro and in vivo protective effects of proteoglycan isolated from mycelia of Ganoderma lucidum on carbon tetrachloride-induced liver injury.

机译:从灵芝菌丝体分离的蛋白聚糖对四氯化碳诱导的肝损伤的体外和体内保护作用。

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AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
机译:目的:探讨从灵芝菌丝体中分离得到的生物活性成分灵芝蛋白聚糖(GLPG)对四氯化碳诱导的肝损伤的保护作用的可能机制。方法:四氯化碳诱导肝损伤模型。 MTT法检测细胞毒性,用多功能生化分析仪测定丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)的活性,并按照SOD的说明测定超氧化物歧化酶(SOD)和TNF-α的水平试剂盒和TNF放射免疫分析试剂盒。肝切片用苏木精和曙红(H和E)染色以进行组织学评估,并在光学显微镜下检查。结果:我们发现GLPG可以通过测量ALT和AST活性来减轻四氯化碳(CCl4)诱导的L-02肝细胞损伤,并且将GLPG给予L-02细胞没有任何毒性。此外,对有或没有GLPG预处理的CCl4诱导的小鼠肝损伤的组织学分析表明,GLPG可以显着抑制CCl4诱导的小鼠肝脏毒性。我们还发现GLPG降低了小鼠血浆中CCl4诱导的TNF-α水平,而增加了大鼠血清中的SOD活性。结论:GLPG在体外和体内均具有抗CCl4诱导的肝损伤的保护作用。可能的抗肝毒性机制可能与TNF-α水平的抑制和自由基清除活性有关。

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