高血压诱导心肌组织内质网应激反应对大鼠心肌细胞凋亡的影响

Effects of stress reaction of endoplasmic reticulum in cardiac muscle tissue induced by hypertension on apoptosis of cardiac muscle cells in rats

目的探讨高血压诱导心肌组织内质网应激反应对大鼠心肌细胞凋亡的影响。方法选择20只自发性高血压大鼠作为观察组,20只普通Wistar-Kyoto大鼠作为对照组,检测2组大鼠血压,并进行超声心动图检测。收集2组大鼠心脏组织标本,检测心肌细胞凋亡率和心肌细胞中活性氧(ROS)含量、GPR78蛋白表达量。结果观察组大鼠血压、室间隔厚度、左心室后壁厚度、二尖瓣E峰最大速度/A峰最大速度比值、心肌细胞凋亡率、ROS荧光强度及心肌细胞GPR78蛋白表达量均明显高于对照组(P均<0.05)。TUNEL凋亡染色观察到观察组心肌组织中存在大量呈棕黄色致密颗粒的凋亡细胞,对照组存在少量浅黄色颗粒;免疫组化染色显示观察组心肌细胞中存在大量浓密深棕色颗粒,对照组中仅存在少量稀疏分布的浅棕色颗粒。结论高血压会导致大鼠出现心肌组织内质网应激反应,并参与心肌细胞凋亡过程,导致心肌内质网应激状态失衡。

Objective It is to explore the effects of stress reaction of endoplasmic reticulum in cardiac muscle tissue induced by hypertension on apoptosis of cardiac muscle cells in rats. Methods 20 spontaneous hypertensive rats as observation group, and 20 normal Wistar Kyoto （WKY） rats as control group, the rats’ blood pressure and indexes of ultrasonic echocar-diography were detected. Cardiac tissue samples were collected to detect the apoptosis rate of myocardial cells, the contents of reactive oxygen species （ ROS） and the expression of GPR78 protein in cardiac muscle cells. Results The blood pressure, thickness of interventricular septum and left ventricular posterior wall, mitral E peak maximum speed/A peak maximum speed ratio,apoptosis rate,ROS fluorescence intensity, and GPR78 protein expression of myocardial cells were significantly higher in observation group than those in control group （F〈0.05）. TUNEL apoptosis staining results showed that there was a large number of apoptotic cells with light yellow compact particles in myocardial tissue in observation group, but a small quantity of light yellow particles was found in control group. Immunohistochemistry staining results showed that there was a large number of densely dark brown compact particles in myocardial tissue in observation group, but a a sparse distribution of shallow brown particles was found in control group. Conclusion Hypertension could induce endoplasmic reticulum stress reaction in the rats, and it was involved in the process of apoptosis, which resulted in the imbalance of endoplasmic reticulum stress.