FAM3A在肝脏缺血再灌注损伤中的保护作用及机制

发布时间：2018-04-16 06:14

本文选题：FAMA + 氧化应激　；参考：《中国病理生理杂志》2015年10期

【摘要】：正目的:研究FAM3A在小鼠肝脏缺血再灌注(IR)损伤中的作用及机制;探索FAM3A是否介导罗格列酮对肝脏缺血再灌注损伤的保护作用。方法和结果:在IR小鼠肝脏中,PPARγ和FAM3A表达增加。利用siRNA敲减肝脏FAM3A后,行IR手术,相较于对照组,敲减FAM3A组血浆AST、ALT水平及氧化应激显著升高,肝脏坏死区域增加,炎症因子及促凋亡因子水平上
[Abstract]:Aim: to investigate the role and mechanism of FAM3A in hepatic ischemia-reperfusion injury in mice, and to explore whether rosiglitazone mediated the protective effect of rosiglitazone on hepatic ischemia-reperfusion injury in mice.Methods and results: the expression of PPAR 纬 and FAM3A increased in the liver of IR mice.Compared with the control group, the plasma alt level and oxidative stress of the knockout FAM3A group were significantly higher than those of the control group, the areas of liver necrosis were increased, and the levels of inflammatory factors and pro-apoptotic factors were increased.
【作者单位】：北京大学医学部;
【分类号】：R575

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