Geriatric Rehabilitation Center, Zhejiang Rehabilitation Medical Center, Hangzhou, Zhejiang, People's Republic of China.
Braz J Cardiovasc Surg. 2022 Oct 8;37(5):727-736. doi: 10.21470/1678-9741-2021-0183.
Coronary heart disease (CHD) is a dynamic process in which there are interactions between endothelial dysfunction, oxidative stress, and inflammatory responses. The aim of the present study was to investigate the function and mechanism of HSCARG in the treatment of CHD.
Male apolipoprotein E/low-density lipoprotein receptor-deficient mice were given a high-fat diet with 21% fat and 0.15% cholesterol for the in vivo model. Human umbilical vein endothelial cells were incubated with angiotensin II for the in vitro model. HSCARG expression was inhibited in patients or mice with CHD.
HSCARG reduced oxidative stress in mice with CHD. HSCARG also reduced reactive oxygen species (ROS)-oxidative stress in the in vitro model. HSCARG induced p47phox expression in the in vitro model by NF-κB activity. The regulation of nuclear factor kappa B (NF-κB) activity or p47phox expression participates in the effects of HSCARG in CHD.
Altogether, our data indicate that HSCARG reduced ROS-oxidative stress in in vivo and in vitro models of CHD via p47phox by NF-κB activity and may be a clinical target for CHD.
冠心病（CHD）是一个动态的过程，其中内皮功能障碍、氧化应激和炎症反应之间存在相互作用。本研究旨在探讨 HSCARG 在 CHD 治疗中的作用和机制。
雄性载脂蛋白 E/低密度脂蛋白受体缺陷小鼠给予含有 21%脂肪和 0.15%胆固醇的高脂肪饮食建立体内模型。体外模型中，人脐静脉内皮细胞用血管紧张素 II 孵育。CHD 患者或小鼠的 HSCARG 表达被抑制。
HSCARG 减少了 CHD 小鼠的氧化应激。HSCARG 还减少了体外模型中的活性氧（ROS）-氧化应激。HSCARG 通过 NF-κB 活性诱导体外模型中的 p47phox 表达。核因子 kappa B（NF-κB）活性或 p47phox 表达的调节参与了 HSCARG 在 CHD 中的作用。
综上所述，我们的数据表明，HSCARG 通过 NF-κB 活性减少了 CHD 体内和体外模型中的 ROS-氧化应激，通过 p47phox 表达，可能是 CHD 的一个临床治疗靶点。
