论文部分内容阅读
内皮细胞功能障碍是造成许多心脑血管疾病的共同病理基础。NO利用率降低和活性氧(ROS)过量生成是导致内皮功能紊乱的一个重要因素。内皮型一氧化氮合酶脱偶联(eNOS uncoupling)是导致NO水平下降和氧自由基水平升高的重要机制,其中ROS水平升高又是造成eNOS脱偶联的主要原因。随着对ROS病理生理作用认识的不断深入,发现ROS的生物学作用具有两面性,一方面ROS与蛋白质、脂质、核酸等生物大分子反应,引发一些病理过程,另一方面ROS通过不同的信号途径对一些生理过程进行调控。该现象主要是由ROS分布的区域化造成。通过抑制ROS合成特异性关键酶减少特定区域内的具体的ROS减少氧化应激、逆转eNOS脱偶联、进而改善血管内皮功能,为防治心脑血管疾病提开辟新的途径。
Endothelial dysfunction is a common pathological basis for many cardiovascular and cerebrovascular diseases. Decreased NO utilization and overproduction of reactive oxygen species (ROS) are an important contributing factor to endothelial dysfunction. Endothelial nitric oxide synthase uncoupling (eNOS uncoupling) is an important mechanism leading to decreased NO levels and elevated levels of oxygen free radicals. ROS levels are the major cause of eNOS uncoupling. With the deepening understanding of the pathophysiology of ROS, we found that the biological role of ROS has two sides. On the one hand, ROS reacts with biological macromolecules such as proteins, lipids and nucleic acids to trigger some pathological processes. On the other hand, Way to regulate some of the physiological processes. This phenomenon is mainly caused by the regionalization of ROS distribution. By inhibiting ROS synthesis-specific key enzyme to reduce specific ROS in specific regions to reduce oxidative stress, reverse eNOS decoupling, thereby improving vascular endothelial function, to open up new ways for the prevention and treatment of cardiovascular and cerebrovascular diseases.