PPARγ激动剂罗格列酮在大鼠肝缺血再灌注损伤中的作用及机制探讨
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Effect of peroxisome proliferator-activated receptor γ activator rosiglitazone in rat hepatic ischemia-reperfusion injury and its mechanism
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    摘要:

    目的:探讨过氧化物酶体增殖物激活受体γ(PPARγ) 激动剂罗格列酮在大鼠肝脏缺血再灌注损伤中的作用及机制。方法:建立70%的大鼠肝脏缺血再灌注损伤模型,SD大鼠随机分为6组,对照组(control,C),假手术组(sham,S),缺血再灌注损伤(ischemia-reperfusion,IR)组,罗格列酮(rosiglitazone ,Ros)预处理组,GW9662预处理组,以及Ros+GW9662预处理组。再灌注后,取静脉血检测肝血清酶(ALT、AST)水平,取肝脏组织TUNEL法检测缺血肝脏细胞凋亡指数(apoptotic index,AI),免疫组化检测Bcl-2,Bax,Caspase-3表达。结果:IR组和Ros组与假手术组相比肝脏细胞凋亡指数、Bax、Bcl-2及Caspase-3均升高。Ros处理组与IR组相比肝脏细胞凋亡指数、Bax及Caspase-3表达降低,Bcl-2表达升高,GW9662能阻断Ros的保护作用。单独应用GW9662时肝脏细胞凋亡指数、Caspase-3以及Bax表达比IR组升高,而Bcl-2降低。结论:PPARγ激动剂罗格列酮对肝脏缺血再灌注损伤有保护作用,它可能是通过上调Bcl-2 表达,下调Bax和Caspase-3表达,抑制肝脏细胞凋亡而起作用的。

    Abstract:

    Objective:To investigate the effect of peroxisome proliferator-activated receptor γ(PPARγ) activator rosiglitazone in rat hepatic ischemia-reperfusion injury and its mechanism. Methods:The model of 70% warm ischemia-reperfusion injury was established in SD rats. Rats were divided randomly into 6 groups:control group, sham group, ischemia-reperfusion group, rosiglitazone group,2-chloro-5-nitrobenzanilide(GW9662) treatment group and rosiglitazone plus GW9662 treatment group. After reperfusion, AST and ALT levels in serum were detected. The liver tissue was removed for measurement of the apoptotic index by TUNEL assay, and the expression of Bax, Bcl-2 and caspase-3 proteins in ischemic hepatocytes were detected by immunohistochemistry. Results:Compared with sham group, the apoptotic index of hepatocytes, expressions of Bax, Bcl-2 and Caspase-3 proteins in ischemia-reperfusion group and rosiglitazone group was greatly increased. Compared with ischemia-reperfusion group, the apoptosis index of hepatocytes, expressions of Bax and Caspase-3 in rosiglitazone group decreased, with Bcl-2 increased. GW9662 abolished the protective effect of rosiglitazone. GW9662 treated alone increased the apoptosis index of hepatocytes, Bax and Caspase-3, with the expression of Bcl-2 decreased. Conclusion:PPARγ activator rosiglitazone could protect against ischemia-reperfusion injury in rats,with its possible mechanism of upregulating the expression of Bcl-2, inhibiting the expression of Bax and Caspase-3, and prohibiting hepatocyte apoptosis.

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曹晓飞,张 峰,张业伟. PPARγ激动剂罗格列酮在大鼠肝缺血再灌注损伤中的作用及机制探讨[J].南京医科大学学报(自然科学版),2007,(11):1271-12731289

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  • 收稿日期:2007-04-19
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