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目的 :研究黄芪甲苷(astragalosideⅣ,As-Ⅳ)对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)引起的线粒体功能障碍的逆转作用。方法:培养大鼠主动脉血管平滑肌细胞(vascular smooth muscle cells,VSMCs),低血清培养液饥饿处理后分为24 h对照组、AngⅡ24 h处理组、48 h对照组、AngⅡ48 h处理组、As-Ⅳ治疗组。24 h对照组和AngⅡ24 h处理组使用线粒体呼吸功能检测仪进行线粒体呼吸功能检测,线粒体ATP含量检测;48 h对照组、AngⅡ48 h处理组和As-Ⅳ治疗组进行线粒体呼吸功能检测、线粒体ATP含量检测、电镜观察线粒体结构变化,共聚焦显微镜检测线粒体内活性氧(reactive oxygen species,ROS)水平和Mn-SOD活性检测。结果:AngⅡ24 h处理组与24 h对照组相比,线粒体耗氧率(oxygen consumption rates,OCRs)出现下降,线粒体ATP含量减少(P≤0.05);AngⅡ48 h处理组与48 h对照组相比,线粒体OCRs显著下降,线粒体ATP含量明显减少(P<0.05),线粒体出现嵴模糊、肿胀、空泡,线粒体内ROS水平升高(P<0.05),Mn-SOD活性下降(P≤0.05);As-Ⅳ治疗组较AngⅡ48 h处理组线粒体OCRs和线粒体ATP含量明显回升(P<0.05),线粒体形态结构损伤减轻,线粒体内ROS水平降低(P<0.05),Mn-SOD活性升高(P≤0.05)。结论 :As-Ⅳ可以通过增强线粒体Mn-SOD活性,降低线粒体内ROS水平,进一步减轻线粒体结构损伤并提高线粒体OCRs和ATP含量,从而逆转AngⅡ引起的线粒体功能障碍。
Objective: To investigate the reversal effect of astragaloside Ⅳ (As-Ⅳ) on mitochondrial dysfunction induced by angiotensin Ⅱ (AngⅡ). Methods: Cultured aortic vascular smooth muscle cells (VSMCs) in rats, and then cultured in low serum medium for 24 h, then treated with Ang Ⅱ 24 h, 48 h, Ang Ⅱ 48 h, As- Ⅳ treatment group. Mitochondrial respiratory function and mitochondrial ATP content were detected by mitochondrial respiratory function detector in 24 h control group and AngⅡ24 h treatment group. Mitochondrial respiratory function was detected in 48 h control group, AngⅡ48 h treatment group and As-Ⅳ treatment group. Mitochondrial ATP content The changes of mitochondrial structure were observed by electron microscope. The levels of reactive oxygen species (ROS) and Mn-SOD in mitochondria were detected by confocal microscopy. Results: Compared with 24 h control group, the oxygen consumption rates (OCRs) of mitochondria and the contents of mitochondrial ATP decreased (P <0.05) in AngⅡ24 h treatment group compared with that of control group at 24 h. Mitochondrial OCRs were significantly decreased, mitochondrial ATP content was significantly decreased (P <0.05), mitochondria cristae were fuzzy, swelling, vacuolization, mitochondrial ROS levels increased (P <0.05), Mn-SOD activity decreased (P <0.05), mitochondrial morphological damage, mitochondrial ROS level decreased (P <0.05) and Mn-SOD activity increased (P≤0.05 ). CONCLUSION: As-IV can reverse mitochondrial dysfunction caused by AngⅡ by increasing mitochondrial Mn-SOD activity, decreasing ROS level in mitochondria, further mitigating mitochondrial structural damage and increasing mitochondrial OCRs and ATP content.