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Vascul Pharmacol. 2009 Aug-Sep;51(2-3):169-74. doi: 10.1016/j.vph.2009.06.004. Epub 2009 Jun 21.

PPAR gamma protects cardiomyocytes against oxidative stress and apoptosis via Bcl-2 upregulation.

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  • 1Department of Cardiology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.


Cardiovascular disease (CVD) is a leading cause of death and disabilities worldwide. Peroxisome proliferator-activated receptor gamma (PPARgamma) agonists possess potent anti-inflammatory actions and have recently emerged as potential therapeutic agents for CVD. Here we show that H2O2 induced apoptosis in cardiomyocytes with a marked down-regulation of Bcl-2 protein. The PPARgamma agonist rosiglitazone protected cardiomyocytes from oxidative stress and apoptosis. Cardiomyocytes constitutively overexpressing PPARgamma were resistant to oxidative stress-induced apoptosis and protected against impairment of mitochondrial function. On the contrary, cells expressing a dominant negative mutant of PPARgamma were highly sensitive to oxidative stress. Cells overexpressing PPARgamma exhibited an almost 3 fold increase in Bcl-2 protein content; whereas, in PPARgamma dominant negative expressing cells, Bcl-2 was barely detected. Bcl-2 knockdown by siRNA in cells overexpressing PPARgamma results in increased sensitivity to oxidative stress, suggesting that Bcl-2 up-regulation mediated the protective effects of PPARgamma. These data suggest that, in oxidative stress-induced cardiomyocyte apoptosis, PPARgamma protects cells from oxidative stress through upregulating Bcl-2 expression. These findings provide further support for the use of PPARgamma agonists in ischemic cardiac disease.

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