南方医科大学学报

南方医科大学学报 ›› 2014, Vol. 34 ›› Issue (02): 197-.

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吡格列酮对大鼠缺血/再灌注心肌过氧化物酶体增殖物受体γ辅激活因子lα表达的影响

申琳，王浩，叶平   

  • 出版日期:2014-02-20 发布日期:2014-02-20

Effects of pioglitazone on myocardial peroxisome proliferator-activated receptor gamma
co-activator lα expression in rats with myocardial ischemia/reperfusion injury

  • Online:2014-02-20 Published:2014-02-20

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摘要： 目的观察吡格列酮对大鼠缺血/再灌注损伤心肌过氧化物酶体增殖物受体γ辅激活因子lα（PGC-lα）表达的影响。方法
24只SD大鼠随机分为4组（n=6）：缺血/再灌注组、吡格列酮5 mg/(kg·d)组、吡格列酮10 mg/（kg·d）组、吡格列酮10 mg/（kg·d）+
过氧化物酶体增殖物激活受体γ（PPARγ）特异性阻断剂GW9662组，利用在体结扎左前降支的方法建立缺血/再灌注损伤模型，
脱氧核糖核苷酸末端转移酶介导的缺口末端标记法（TUNEL法）检测心肌细胞凋亡，RT-PCR方法检测心肌组织PGC-lα mRNA
的变化，Western blot检测心肌组织PGC-lα蛋白的变化。结果TUNEL法显示吡格列酮抑制缺血/再灌注心肌细胞凋亡[（21.4±
8.8）%、（17.3±8.7）%、（40.1±12.3）%，P<0.05）]，吡格列酮上调PGC-lα表达（P<0.05），GW9662逆转吡格列酮对凋亡细胞的抑制
作用（P<0.05），抑制吡格列酮促进PGC-lα表达上调的作用（P<0.05）。结论吡格列酮抑制缺血/再灌注损伤诱导的心肌细胞凋
亡，吡格列酮促进PGC-lα上调，这两种作用是由PPARγ介导的。

Abstract: Objective To investigate the effects of pioglitazone on the expression of peroxisome proliferator-activated receptor
gamma co-activator lα (PGC-lα) in rat myocardium following myocardial ischemia/reperfusion (I/R) injury. Methods
Twenty-four SD rats were randomly divided into 4 equal groups, namely I/R group, pioglitazone (5 mg/kg daily) group,
pioglitazone (10 mg/kg daily) group, and pioglitazone (10 mg/kg) + peroxisome proliferator-activated receptor γ
(PPARγ)-specific antagonist GW9662 group. Myocardial I/R injury was induced by ligation of the left anterior descending
coronary artery for 30 min and reperfusion for 120 min. Myocardial apoptosis following I/R injury was examined with TUNEL
assay; RT-PCR and Western blotting were employed to detect the expression of PGC-lα mRNA and protein, respectively.
Results Pioglitazone treatment significantly suppressed myocardial apoptosis (21.4%±8.8%、17.3%±8.7%、40.1%±12.3%, P<0.05)
following I/R injury and up-regulated myocardial PGC-lα expression at both the mRNA and protein levels (P<0.05), but these
effects were antagonized by GW9662 (P<0.05). Conclusion Pioglitazone can inhibit myocardial apoptosis induced by I/R injury
and up-regulate myocardial PGC-lα expression, and these effects are mediated by PPARγ.