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目的:研究黄芪甲苷对肾血管性高血压大鼠主动脉内皮细胞线粒体损伤的保护作用。方法:采用两肾一夹制备肾血管性高血压大鼠,术后2周将大鼠随机分为手术组和黄芪甲苷治疗组[5.0 mg/(kg·d)],以假手术组为正常对照,治疗2周后,观察大鼠胸主动脉内皮细胞线粒体超微结构的变化,应用免疫组化染色法观察大鼠胸主动脉内皮细胞锰超氧化物歧化酶(SOD2)的表达。结果:术后2周大鼠收缩压明显高于正常对照大鼠。手术组大鼠胸主动脉内皮细胞线粒体内嵴断裂、消失,基质电子密度降低,肿胀、空泡化明显;黄芪甲苷治疗后大鼠胸主动脉内皮细胞线粒体损伤程度明显减轻。手术组大鼠胸主动脉内皮细胞SOD2表达水平较正常对照大鼠明显降低,黄芪甲苷治疗后恢复至正常大鼠水平。结论:黄芪甲苷对肾血管性高血压大鼠主动脉内皮细胞线粒体的损伤有保护作用,上调主动脉内皮细胞SOD2表达是其可能途径之一。
Objective: To study the protective effects of astragaloside on mitochondrial damage of aortic endothelial cells in renovascular hypertensive rats. Methods: Renal vascular hypertensive rats were established by two kidneys and one clip. The rats were randomly divided into operation group and Astragaloside treatment group [5.0 mg / (kg · d)] two weeks after operation. The rats in sham operation group were After 2 weeks of treatment, the changes of mitochondrial ultrastructure in the thoracic aorta endothelial cells were observed. The expression of manganese superoxide dismutase (SOD2) in rat thoracic aorta endothelial cells was observed by immunohistochemical staining. Results: The systolic pressure of rats after 2 weeks was obviously higher than that of normal control rats. The thoracic aorta endothelial cells mitochondrial cristae were ruptured and disappeared in the operation group, the stromal electron density was reduced, swelling and vacuolization were obvious. The mitochondrial damage of thoracic aorta endothelial cells in astragaloside treatment group was relieved. The expression level of SOD2 in the thoracic aorta endothelial cells in the operation group was significantly lower than that in the normal control group, and recovered to the normal level after treatment with astragaloside IV. CONCLUSION: Astragaloside has a protective effect on mitochondria of aortic endothelial cells in renovascular hypertensive rats. Up-regulation of SOD2 expression in aortic endothelial cells is one of the possible ways.