• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Acetylcholine Attenuates Hypoxia/ Reoxygenation-Induced Mitochondrial and Cytosolic ROS Formation in H9c2 Cells via M2 Acetylcholine Receptor
【24h】

Acetylcholine Attenuates Hypoxia/ Reoxygenation-Induced Mitochondrial and Cytosolic ROS Formation in H9c2 Cells via M2 Acetylcholine Receptor

机译：乙酰胆碱通过M2乙酰胆碱受体减轻H9c2细胞中缺氧/复氧诱导的线粒体和胞质ROS的形成

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

biBackground /i/bThe anti-infammatory and cardioprotective effect of acetylcholine (ACh) has been reported; nevertheless, whether and how ACh exhibits an antioxidant property against ischemia/reperfusion (I/R)-induced oxidative stress remains obscure. biMethods /i/bIn the present study, H9c2 rat cardiomyocytes were exposed to hypoxia/reoxygenation (H/R) to mimic I/R injury. We estimated intracellular different sources of reactive oxygen species (ROS) by measuring mitochondrial ROS (mtROS), mitochondrial DNA (mtDNA) copy number, xanthine oxidase (XO) and NADPH oxidase (NOX) activity and expression of rac 1. Cell injury was determined by lactate dehydrogenase (LDH) release and cleaved caspase-3 expression. The siRNA transfection was performed to knockdown of M2 acetylcholine receptor (M2 AChR) expression. biResults /i/b12-h hypoxia followed by 2-h reoxygenation resulted in an abrupt burst of ROS in H9c2 cells. Administration of ACh reduced the levels of ROS in a concentration-dependent manner. Compared to the H/R group, ACh decreased mtROS, recovered mtDNA copy number, diminished XO and NOX activity, rac 1 expression as well as cell injury. Co- treatment with atropine rather than hexamethonium abolished the antioxidant and cardioprotective effect of ACh. Moreover, knockdown of M2 AChR by siRNA showed the similar trends as atropine co-treatment group. biConclusions /i/bACh inhibits mitochondria-, XO- and NOX-derived ROS production thus protecting H9c2 cells against H/R-induced oxidative stress, and these benefcial effects are mainly mediated by M2 AChR. Our findings suggested that increasing ACh release could be a potential therapeutic strategy for treatment and prevention of I/R injury.
机译：背景 已经报道了乙酰胆碱（ACh）的抗消炎和心脏保护作用;但是，乙酰胆碱酯是否以及如何表现出抗缺血/再灌注（I / R）诱导的氧化应激的抗氧化性能仍然不清楚。 方法 在本研究中，将H9c2大鼠心肌细胞暴露于缺氧/复氧（H / R）以模拟I / R损伤。我们通过测量线粒体ROS（mtROS），线粒体DNA（mtDNA）拷贝数，黄嘌呤氧化酶（XO）和NADPH氧化酶（NOX）活性以及rac 1的表达来估计细胞内不同活性氧（ROS）的来源。通过乳酸脱氢酶（LDH）的释放和裂解的caspase-3表达。进行siRNA转染以敲低M2乙酰胆碱受体（M2 AChR）表达。 结果 12小时缺氧，然后再进行2小时再充氧导致H9c2细胞中的ROS突然爆发。 ACh的给药以浓度依赖的方式降低了ROS的水平。与H / R组相比，ACh降低了mtROS，恢复了mtDNA拷贝数，减少了XO和NOX活性，降低了rac 1的表达以及细胞损伤。与阿托品而不是六甲铵的共同治疗消除了乙酰胆碱的抗氧化和心脏保护作用。此外，通过siRNA敲低M2 AChR表现出与阿托品联合治疗组相似的趋势。 结论 ACh抑制线粒体，XO和NOX产生的ROS，从而保护H9c2细胞免受H / R诱导的氧化应激的影响，这些有益作用主要由M2介导。 AChR。我们的发现表明，增加ACh释放可能是治疗和预防I / R损伤的潜在治疗策略。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号