文章摘要
张少君,吴恒芳,陈相健,杨 笛,朱铁兵.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[J].南京医科大学学报,2014,(7):889~893
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
Effect of astragaloside Ⅳ on mitochondrial injury of aortic endothelial cells from renovascular hypertensive rats
投稿时间:2014-02-28  
DOI:10.7655/NYDXBNS20140707
中文关键词: 黄芪甲苷  肾血管性高血压大鼠  主动脉内皮细胞  线粒体  锰超氧化物歧化酶
英文关键词: astragaloside Ⅳ  renovascular hypertensive rats  aortic endothelial cells  mitochondria  Mn-superoxide dismutase (SOD2)
基金项目:国家自然科学基金(81170220;81100156)
作者单位
张少君 南京医科大学第一附属医院心血管内科,江苏 南京 210029 
吴恒芳 南京医科大学第一附属医院心血管内科,江苏 南京 210030 
陈相健 南京医科大学第一附属医院心血管内科,江苏 南京 210031 
杨 笛 南京医科大学第一附属医院心血管内科,江苏 南京 210032 
朱铁兵 南京医科大学第一附属医院心血管内科,江苏 南京 210033 
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中文摘要:
      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?
英文摘要:
      Objective:The present study was designed to investigate the protective effect of astragaloside IV on mitochondrial injury of aortic endothelial cells from renovascular hypertensive rats. Methods:Two kidney one clip (2K1C) technique was performed to prepare renovascular hypertensive rats. Two weeks after operation,the rats were divided into two groups,the operation group and the astragaloside Ⅳ treatment group[5.0 mg/(kg?d)]. The sham operated rats were used as normal control. After treatment for two weeks,the mitochondrial ultrastructure of thoracic aortic endothelial cells from the rats was observed. The expression of Mn-superoxide dismutase (SOD2) in thoracic aortic endothelium was observed by immunohistochemical staining. Results:Two weeks after operation,the rats showed significant increase of systolic blood pressure compared to that of control rats. The thoracic aortic endothelial cell mitochondria of hypertensive rats showed fracture and disappearance of cristae,swelling and vacuolation as well as decreased mitochondrial matrix electron density. These changes of mitochondrial were ameliorated significantly by astragaloside Ⅳ. In addition,astragaloside Ⅳ augmented the lower expression level of SOD2 in the aortic endothelium from the hypertensive rats compared with that from the normal controls. Conclusion:Astragaloside Ⅳ reverses mitochondrial injury of aortic endothelial cells from renovascular hypertensive rats,which may be linked to its ability to increase SOD2 expression in the aortic endothelium of the rats.
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