论文部分内容阅读
目的本研究旨在观察注射用血栓通对肝损伤的防治效果,并初步探讨其发挥药效的机制。方法将0.6mmol/L的H2O2加入到10-7～102μg/ml的经注射用血栓通预处理HepG2细胞中,四甲基偶氮唑盐(MTT)观察细胞活力;10%CCl4腹腔注射于经注射用血栓通(50mg/kg、5mg/kg、0.5mg/kg)预处理的SD大鼠,于注射CCl4的24、48、72h动态观察大鼠血清ALT、AST、TBil的变化,并于实验结束取大鼠肝组织进行组织学检查;HepG2细胞经10-3μg/ml注射用血栓通作用48h,提取mRNA,逆转录成cDNA,与芯片杂交,根据基因芯片杂交信号强弱筛选相关基因。结果注射用血栓通处理的HepG2细胞受到H2O2损伤时能够维持细胞的活力状态;注射用血栓通可以抑制CCl4造成肝损伤时血清ALT、AST、TBil的升高,并减轻肝损伤时大鼠肝组织的病理改变;注射用血栓通的肝细胞损伤保护作用可能与上调肝细胞损伤修复基因有关。结论注射用血栓通能够抑制H2O2造成的肝细胞损伤,抑制CCl4造成的大鼠肝损伤,其机制可能与其上调某些损伤修复基因的表达及/或下调某些损伤相关基因表达有关。
Objective The purpose of this study was to observe the effect of Xueshuantong injection on the prevention and treatment of liver injury, and to explore the mechanism of its efficacy. Methods 0.6mmol/L H2O2 was added to 10-7～102μg/ml HepG2 cells pretreated by thrombosis. MTT was used to observe the cell viability. 10% CCl4 was intraperitoneally injected into the mesenchymal stem cells. The serum ALT, AST, and TBil levels in rats were pretreated with Xueshuantong (50mg/kg, 5mg/kg, 0.5mg/kg) for 24, 48, and 72h after CCl4 injection. The hepatic tissue of rats was taken for histological examination; HepG2 cells were treated with 10-3μg/ml thrombus for 48 hours, and mRNA was extracted, reverse transcribed into cDNA, and hybridized with the chip. The related genes were screened according to the strength of the gene chip hybridization signal. Results The thromboxane-treated HepG2 cells could maintain the vitality of the cells when injured by H2O2; Injection Xueshuantong could inhibit the increase of serum ALT, AST and TBil in the liver injury caused by CCl4, and reduce the hepatic tissue in liver injury. The pathological changes; hepatocyte injury protection of injection Xueshuantong may be related to up-regulation of hepatocyte injury repair genes. Conclusion Xueshuantong injection can inhibit the hepatocyte injury caused by H2O2 and inhibit the liver damage induced by CCl4 in rats. The mechanism may be related to up-regulation of the expression of some repair genes and/or down-regulation of some damage-related gene expressions.