黄芪甲苷逆转血管紧张素Ⅱ引起的主动脉平滑肌细胞线粒体功能障碍
作者:
作者单位:

作者简介:

通讯作者:

中图分类号:

基金项目:

国家自然科学基金(81170220,81100156)


Astragaloside Ⅳ ameliorates mitochondrial dysfunction of vascular smooth muscle cells induced by angiotensin Ⅱ in rats
Author:
Affiliation:

Fund Project:

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    目的:研究黄芪甲苷(astragaloside Ⅳ,As-Ⅳ)对血管紧张素Ⅱ(angiotensin Ⅱ,Ang Ⅱ)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-Ang Ⅱ 24 h 处理组-48 h 对照组-Ang Ⅱ 48 h 处理组-As-Ⅳ 治疗组-24 h 对照组和Ang Ⅱ 24 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-Ang Ⅱ 48 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:Ang Ⅱ 24 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);Ang Ⅱ 48 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 Ang Ⅱ 48 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Ang Ⅱ引起的线粒体功能障碍-

    Abstract:

    Objective:To investigate the reverse effect of astragaloside Ⅳ (As-Ⅳ) on angiotensin Ⅱ (Ang Ⅱ)-induced mitochondrial dysfunction of vascular smooth muscle cells (VSMCs) in rats. Methods: Cultured VSMCs were divided into the 24 h control group, the Ang Ⅱ treated for 24 h group, the 48 h control group, the Ang Ⅱ treated for 48 h group,and the As-Ⅳ treated group. After treatment, the 24 h control group and the Ang Ⅱ treated for 24 h group were tested for mitochondrial function by Extracellular Flux Analyzer and mitochondrial ATP production. The 48 h control group, the Ang Ⅱ treated for 48 h group,and the As-Ⅳ treated group were tested for mitochondrial function, mitochondrial ATP production, mitochondrial morphology by transmission electron microscope, and reactive oxygen species (ROS) production by confocal microscopy and Mn-SOD activity. Results: Compared with the 24 h controls group, oxygen consumption rates (OCRs) and mitochondrial ATP production decreased in the Ang Ⅱ treated for 24 h group (P ≤ 0.05); Compared with the 48 h controls group, the Ang Ⅱ treated for 48 h group showed a decrease of OCRs and mitochondrial ATP production (P ≤ 0.05), swollen and vacuolization of mitochondrial morphology with almost wash-out cristae, a decrease of Mn-SOD activity (P ≤ 0.05) and a increase of mtROS level (P ≤ 0.05). The As-Ⅳ treatment group showed significantly increased OCRs, mitochondrial ATP production (P ≤ 0.05) and Mn-SOD activity (P ≤ 0.05), decreased mtROS level (P ≤ 0.05), and reduced damage of mitochondrial morphology compared with the Ang Ⅱ treated for 24 h group. Conclusion: This study demonstrates that As-Ⅳ could reverse Ang Ⅱ induced mitochondrial dysfunction of VSMCs by enhancing Mn-SOD activity to decrease mtROS production, further alleviating the damage of mitochondrial morphology and increasing OCRs and mitochondrial ATP production.

    参考文献
    相似文献
    引证文献
引用本文

路 遥,徐晋妉,卞智萍,吴恒芳,顾春荣,陈相健,杨 笛.黄芪甲苷逆转血管紧张素Ⅱ引起的主动脉平滑肌细胞线粒体功能障碍[J].南京医科大学学报(自然科学版),2015,(7):975-980

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2015-03-24
  • 最后修改日期:
  • 录用日期:
  • 在线发布日期: 2015-07-12
  • 出版日期:
通知关闭
郑重声明