本文選題：FAMA + 氧化應(yīng)激��； 參考：《中國(guó)病理生理雜志》2015年10期

【摘要】：正目的:研究FAM3A在小鼠肝臟缺血再灌注(IR)損傷中的作用及機(jī)制;探索FAM3A是否介導(dǎo)羅格列酮對(duì)肝臟缺血再灌注損傷的保護(hù)作用。方法和結(jié)果:在IR小鼠肝臟中,PPARγ和FAM3A表達(dá)增加。利用siRNA敲減肝臟FAM3A后,行IR手術(shù),相較于對(duì)照組,敲減FAM3A組血漿AST、ALT水平及氧化應(yīng)激顯著升高,肝臟壞死區(qū)域增加,炎癥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 緯 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.
【作者單位】： 北京大學(xué)醫(yī)學(xué)部;
【分類號(hào)】：R575

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1 陳真真;賈石;管又飛;楊吉春;;FAM3A刺激血管平滑肌細(xì)胞增殖和遷移的機(jī)制研究[A];中國(guó)生理學(xué)會(huì)第十屆全國(guó)青年生理學(xué)工作者學(xué)術(shù)會(huì)議論文摘要[C];2013年

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