鬼针聚炔苷对CCl4诱导的小鼠急性肝损伤的保护作用

摘要

Objective To study the protective effect of bipinnatpolyacetylenicloside on acute liver injury induced by CCl4in mice. Methods Mice were divided into 6 groups including control group, model group, positive group Silymarin, and bipinnatpolyacetylenicloside treatment(12.5,25,50 mg · kg-1 ) group. Acute hepatic injury was induced by injecting 0. 1ml( 10g)-1 0.2% olive oil solution of carbon tetrachloride and mice in bipinnatpolyacetylenicloside treatment group were intragastric administered with bipinnatpolyacetylenicloside for 6 days before given carbon tetrachloride. Serum AST and ALT were detemined. The contents of SOD, GSH-Px , MDA, and NO in liver homogenate were determined. The index as well as the histopathological test of liver was observed and the expression of NF-ΚB p65 in liver was tested by immunohistochemistry. Results Compared with those in model group, the levels of AST, ALT in serum, the contents of MDA, NO in liver homogenate were reduced significantly while the levels of SOD, GSH-Px in liver homogenate were markedly increased. In bipinnatpolyacetylenicloside treatment (12. 5,25,50 mg ·kg-1) groups, histopathological study showed that the degenerative and necrotic liver cells could be evidently ameliorated , and, immunohistochemistry research demonstrated that the expression of NF-ΚB was dramatically decreased. Conclusion The bipinnatpolyacetylenicloside has a protective effect on the carbon tetrachloride induced acute liver injury in mice, the mechanism of which may be related to its antioxidant characteristic as well as the production of NO and the expression of NF-ΚB being inhibited.%目的 研究鬼针聚炔苷(BPC)对CCl4诱导的小鼠急性肝损伤的保护作用.方法 腹腔注射0.2%CCl4橄榄油溶液建立小鼠急性肝损伤模型,以水飞蓟素为阳性对照,鬼针聚炔苷(12.5、25、50 mg·kg-1)灌胃给药6 d,测定各组小鼠血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)的含量;检测肝组织匀浆中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性和丙二醛(MDA)、一氧化氮(NO)的含量;同时计算肝指数、并对肝组织进行病理组织学检查,免疫组化学法观察NF-κB p65在肝组织中的表达.结果 与模型组比较,鬼针聚炔苷能够显著降低血清ALT、AST的含量;提高肝组织中SOD、GSH-Px的水平,降低MDA、NO的含量;能明显改善肝细胞变性和坏死;可以显著减少NF-κBP65的表达.结论 BPC对CCl4所致小鼠急性肝损伤有保护作用,其机制町能与抗脂质过氧化、抑制NO产生及抑制NF-κB表达等有关.