Capsaicin Protects Cardiomyocytes against Anoxia/Reoxygenation Injury via Preventing Mitochondrial Dysfunction Mediated by SIRT1.
Capsaicin Protects Cardiomyocytes against Anoxia/Reoxygenation Injury via Preventing Mitochondrial Dysfunction Mediated by SIRT1.
复制标题
辣椒素通过预防 SIRT1 介导的线粒体功能障碍来保护心肌细胞免受缺氧/复氧损伤
DOI：
10.1155/2017/1035702
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发表时间：
2017
影响因子：
--
通讯作者：
He M
中科院分区：
文献类型：
--
作者：
He H;Zhou Y;Huang J;Wu Z;Liao Z;Liu D;Yin D;He M
辣椒素(Capsaicin，Cap)已被报道对心血管系统有有益的影响，但这些影响的机制仍不清楚。细胞凋亡与线粒体功能障碍有关，上调SIRT1的表达可抑制缺氧/复氧(A/R)诱导的心肌细胞凋亡。因此，本研究的目的是验证Cap对心肌细胞损伤的保护作用是否由SIRT1介导。观察CAP与SIRT1抑制剂水飞蓟醇合用与否对缺氧/复氧诱导的原代新生大鼠心肌细胞存活率、乳酸脱氢酶(LDH)、肌酸磷酸激酶(CPK)活性、细胞内活性氧(ROS)水平、线粒体膜电位(MMPs)、相关蛋白表达、线粒体通透性转换孔(MPTP)开放及凋亡率的影响。CAP能显著提高心肌细胞存活率，上调SIRT1和Bcl2的表达，减少心肌细胞LDH和CPK的释放，ROS的产生，基质金属蛋白酶的丧失，MPTP的开放，caspase-3的活性，细胞色素c的释放，以及心肌细胞的凋亡。Sirtinol可显著阻断Cap的心脏保护作用。结果提示，Cap对A/R所致心肌细胞损伤的保护作用与SIRT1有关。
Capsaicin (Cap) has been reported to have beneficial effects on cardiovascular system, but the mechanisms underlying these effects are still poorly understood. Apoptosis has been shown to be involved in mitochondrial dysfunction, and upregulating expression of SIRT1 can inhibit the apoptosis of cardiomyocytes induced by anoxia/reoxygenation (A/R). Therefore, the aim of this study was to test whether the protective effects of Cap against the injury to the cardiomyocytes are mediated by SIRT1. The effects of Cap with or without coadministration of sirtinol, a SIRT1 inhibitor, on changes induced by A/R in the cell viability, activities of lactate dehydrogenase (LDH), creatine phosphokinase (CPK), levels of intracellular reactive oxygen species (ROS), and mitochondrial membrane potential (MMP), related protein expression, mitochondrial permeability transition pore (mPTP) opening, and apoptosis rate in the primary neonatal rat cardiomyocytes were tested. Cap significantly increased the cell viability, upregulated expression of SIRT1 and Bcl-2, and decreased the LDH and CPK release, generation of ROS, loss of MMP, mPTP openness, activities of caspase-3, release of the cytochrome c, and apoptosis of the cardiomyocytes. Sirtinol significantly blocked the cardioprotective effects of Cap. The results suggest that the protective effects of Cap against A/R-induced injury to the cardiomyocytes are involved with SIRT1.