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首页> 外文期刊>Journal of Cellular Physiology >Rosiglitazone and PPAR-gamma overexpression protect mitochondrial membrane potential and prevent apoptosis by upregulating anti-apoptotic Bcl-2 family proteins.
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Rosiglitazone and PPAR-gamma overexpression protect mitochondrial membrane potential and prevent apoptosis by upregulating anti-apoptotic Bcl-2 family proteins.

机译：罗格列酮和超表达γ- ppar保护线粒体膜电位和防止被上调抗凋亡细胞凋亡bcl - 2家族蛋白质。

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摘要

To determine the involvement of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) in cytoprotection, we subjected N2-A cells to oxygen-glucose deprivation followed by reoxygenation (H-R). Following H-R insults, H(2)O(2) production was increased while cell viability declined, which was accompanied by loss of mitochondrial membrane potential (MMP), cytochrome c release, caspases 9 and 3 activation, poly(ADP-ribose)polymerase (PARP) cleavage and apoptosis. Rosiglitazone up to 5 microM protected cell viability, normalized MMP, and prevented apoptotic signals. The protective effect of rosiglitazone was abrogated by GW9662, a PPAR-gamma antagonist, or a specific PPAR-gamma small interference RNA (siRNA) but not a control scRNA. PPAR-gamma overexpression alone was effective in maintaining MMP and preventing apoptosis and its protective effect was also abrogated by PPAR-gamma siRNA or GW9662. To elucidate the mechanism by which PPAR-gamma protects MMP and prevents apoptosis, we analyzed Bcl-2, Bcl-xl, and phosphorylated Bad (p-Bad). H-R suppressed them. Rosiglitazone or PPAR-gamma overexpression restored them via PPAR-gamma. Rosiglitazone or PPAR-gamma overexpression preserved phosphorylated Akt and 3-phosphoinositide-dependent kinase-1 (PDK-1) in a PPAR-gamma dependent manner. These results indicate that ligand-activated PPAR-gamma protects N2-A cells against H-R damage by enhancing Bcl-2/Bcl-xl and maintaining p-Bad via preservation of p-Akt.
机译：确定过氧物酶体的参与proliferator-activated receptor-gamma()γ- ppar cytoprotection,我们遭受N2-A细胞oxygen-glucose剥夺紧随其后复氧(H-R)。H (2) O(2)产量增加而细胞生存能力下降,伴随着损失线粒体膜电位(MMP),细胞色素c的释放,还存在9和3激活,保利(ADP-ribose)聚合酶(PARP)分裂和细胞凋亡。规范化MMP的microM保护细胞的生存能力,和阻止凋亡信号。罗格列酮的影响被GW9662废除,特定- ppar - ppar拮抗剂或小干扰RNA (siRNA)而不是控制scRNA。有效地维持MMP和预防细胞凋亡及其保护作用也由核或GW9662γ- ppar废除。阐明- ppar的机制保护MMP和防止细胞凋亡,我们分析bcl - 2、Bcl-xl和磷酸化坏(p-Bad)。H-R镇压他们。通过- ppar超表达恢复它们。罗格列酮或超表达γ- ppar保存磷酸化Akt和3-phosphoinositide-dependent激酶1 (PDK-1)- ppar依赖的方式。表明ligand-activated - ppar保护对H-R N2-A细胞损伤加强bcl - 2 / Bcl-xl和维护p-Bad通过p-Akt保存。

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