Inhibiting Cytochrome C Oxidase Leads to Alleviated Ischemia Reperfusion Injury.
Inhibiting Cytochrome C Oxidase Leads to Alleviated Ischemia Reperfusion Injury.
复制标题
抑制细胞色素 C 氧化酶可减轻缺血再灌注损伤
DOI：
10.4070/kcj.2016.0137
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发表时间：
2017-03
影响因子：
2.9
通讯作者：
Liu L
中科院分区：
文献类型：
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作者：
Yang Z;Duan Z;Yu T;Xu J;Liu L
本研究的总体目的是探讨细胞色素C氧化酶（CcO）通过气体信号分子途径预防缺血再灌注引起的心脏损伤的作用。我们使用CcO抑制剂氰化钾（KCN）模拟大鼠全身缺血再灌注（IR）损伤模型中气体信号分子的预处理。通过测定线粒体H2O2和线粒体复合体活性来测定细胞内活性氧（ROS）。KCN预处理可减少IR损伤后梗死面积，改善心功能。IR损伤KCN预处理组通过抑制活性而非下调CcO表达来减少ROS的产生。此外，KCN预处理与线粒体抗氧化酶的表达和活性增强相关，提示CcO通过氧化应激调节IR损伤。KCN预处理降低了IR损伤的严重程度。其潜在机制可能是增加内源性抗氧化酶活性，从而增强对活性氧的清除。
The overall purpose of this study was to investigate the role of cytochrome C oxidase (CcO) in preventing ischemia reperfusion-induced cardiac injury through gaseous signaling molecule pathways. We used CcO inhibitor, potassium cyanide (KCN) to mimic the pre-treatment of gaseous signaling molecules in a global ischemia/reperfusion (IR) injury model in rats. Intracellular reactive oxygen species (ROS) was determined by measuring mitochondrial H2O2 and mitochondrial complex activity. KCN pre-treatment led to decreased infarction area after IR injury and improved cardiac function. KCN pre-treated group challenged with IR injury was associated with reduced ROS production through inhibition of activity and not downregulation of CcO expression. In addition, KCN pre-treatment was associated with enhanced expression and activity of mitochondrial antioxidase, suggesting the role of CcO in regulating IR injury through oxidative stress. KCN pre-treatment reduced the severity of IR injury. The potential mechanism could be increased endogenous anti-oxidase activity and consequently, the enhanced clearance of ROS.