摘要
Background Whether pre-treatment with peroxisome proliferator activated receptor-γ （PPAR-γ） agonist has beneficial effect on myocardial ischemia / reperfusion （I/R） injury is not well established. In this study, we try to explore the cardioprotective effect of the pre-treatment with PPAR-γ agonist rosiglitazone （Ros） on the hearts suffering I/R injury. Methods Experimental I/R injury was induced by Langendorff heart reperfusion model and left anterior descending artery ligation in rats. Oxidative stress was evaluated by measuring lactate dehydrogenase （LDH）, nitric oxide synthase （NOS）, superoxide dismutase （SOD） and malonaldehyde （MDA）. Bcl-2 and Bax were detected by Western blotting and real-time PCR. Results Ros treatment significantly decreased SOD and inducible nitric oxide synthase and increased creatine kinase, LDH, MDA, and endothelial nitric oxide synthase in-vivo. Both in vitro and in-vivo, Ros treatment increased Bcl-2 level and decreased Bax level in a dose-dependent manner. In vitro, Ros treatment significantly increased SOD but lowered MDA and LDH in a dose-dependent manner. Conclusions Pre-treatment with PPARγ agonist Ros has beneficial effect on myocardial I/R injury by attenuating oxidative stress and inhibiting cardiomyocyte apoptosis.
Background Whether pre-treatment with peroxisome proliferator activated receptor-γ （PPAR-γ） agonist has beneficial effect on myocardial ischemia / reperfusion （I/R） injury is not well established. In this study, we try to explore the cardioprotective effect of the pre-treatment with PPAR-γ agonist rosiglitazone （Ros） on the hearts suffering I/R injury. Methods Experimental I/R injury was induced by Langendorff heart reperfusion model and left anterior descending artery ligation in rats. Oxidative stress was evaluated by measuring lactate dehydrogenase （LDH）, nitric oxide synthase （NOS）, superoxide dismutase （SOD） and malonaldehyde （MDA）. Bcl-2 and Bax were detected by Western blotting and real-time PCR. Results Ros treatment significantly decreased SOD and inducible nitric oxide synthase and increased creatine kinase, LDH, MDA, and endothelial nitric oxide synthase in-vivo. Both in vitro and in-vivo, Ros treatment increased Bcl-2 level and decreased Bax level in a dose-dependent manner. In vitro, Ros treatment significantly increased SOD but lowered MDA and LDH in a dose-dependent manner. Conclusions Pre-treatment with PPARγ agonist Ros has beneficial effect on myocardial I/R injury by attenuating oxidative stress and inhibiting cardiomyocyte apoptosis.
基金
supported by the National Natural Science Foundation of China(No.81301676)
Guangdong Province Natural Science Fund(S2011010002650)
Guangdong Provincial Science and Technology Projects(No.2012B031800293)
the PhD Start-up program of Guangdong Province Natural Science Fund(No.S2012040008047)
