中国医科大学学报

中国医科大学学报

中国医科大学学报 ›› 2012, Vol. 41 ›› Issue (6): 517–521.

• 基础医学 • 上一篇    下一篇

血管周围脂肪组织中AngⅡ介导VSMCs增殖的机制

史吉莹,刘唐威,杨国勋,黄江南,宋梦莹,钱静   

  1. (广西医科大学第一附属医院高血压病区,南宁 530021)
  • 收稿日期:2012-09-25 修回日期:2012-09-25 出版日期:2012-06-20 发布日期:2012-09-27

The Mechanism of Ang-mediatedⅡVSMCs Proliferation in Perivascular Adipose Tissue

SHI Ji-ying, LIU Tang-wei, YANG Guo-xun, HUANG Jiang-nan, SONG Meng-ying, QIAN Jing   

  1. (Department of Hypertension, The First Affiliated Hospital, Guangxi Medical University, Nanning 530021, China)
  • Received:2012-09-25 Revised:2012-09-25 Online:2012-06-20 Published:2012-09-27

摘要: 目的 探讨血管周围脂肪组织(PVAT)中血管紧张素Ⅱ(AngⅡ)介导血管平滑肌细胞(VSMC)增殖的相关机制。方法 培养大鼠平滑肌细胞,MTT试验检测AngⅡ处理后细胞增殖率,检测AngⅡ处理后活性氧(ROS)、H2O2及HOCL水平; 预先给予NADPH抑制剂(apocynin)、H2O2水解酶(catalase)、ERK1/2抑制剂(PD98059)分别作用于AngⅡ处理的细胞,观察其对细胞总蛋白、细胞周期的影响,并检测H2O2及HOCL含量的变化。结果 AngⅡ(终浓度100 nmol/L)处理24 h后细胞与未予AngⅡ处理比较可明显诱导细胞增殖(P<0.05),且ROS随着升高;预先给予NADPH抑制剂apocynin、H2O2水解酶catalase、ERK1/2抑制剂PD98059分别作用于AngⅡ处理的细胞与单用AngⅡ处理的细胞比较可抑制细胞增殖(P<0.05);预先给予NADPH抑制剂(apocynin)、H2O2水解酶(catalase)与单用AngⅡ处理的细胞比较可降低H2O2及HOCL含量(P<0.05),但ERK1/2抑制剂(PD98059)与单用AngⅡ处理组比较无此效应(P>0.05)。结论 在PVAT中ROS在介导AngⅡ诱导VSMCs增殖的通路可能为Nox/H2O2/HOCL/ERK1/2。

关键词: 血管周围脂肪组织, 活性氧, 血管紧张素Ⅱ, 血管平滑肌细胞, 过氧化氢, 次氯酸

Abstract: Objective To investigate the mechanism of vascular smooth muscle cells (VSMC) proliferation induced by AngⅡin perivascular adipose tissue (PVAT). Methods Rat aortic smooth muscle cells were cultured. Smooth muscle cellular proliferatial rate was determined by MTT assay. ROS, H2O2 and HOCL were detected after the treatment with AngⅡ. NADPH inhibitor (apocynin), H2O2 enzymes (catalase), ERK1/2 inhibitor(PD98059) were treated respectively before the AngⅡ treatment on cells. Then the total cellular protein, cell cycle, the content of H2O2 and HOCL were tested. Results Twenty four hours later after treatment with100nM Ang Ⅱ, proliferation and the increase of ROS were more obvious in cells with Ang Ⅱ treatment than the normal group. NADPH inhibitor (apocynin), H2O2 enzymes (catalase) and ERK1/2inhibitor(PD98059) inhibited cell proliferation. And NADPH inhibitor (apocynin) and H2O2 enzymes (catalase) reduced the level of H2O2 and HOCL. However, the ERK1/2 inhibitor (PD98059) showed no such effect. Conclusion In PVAT, the pathway of ROS in mediating the proliferation of VSMCs induced by AngⅡmay be Nox/H2O2/HOCL/ERK1/2.

Key words: perivascular adipose tissue, reactive oxygen species, angiotensin Ⅱ, vascular smooth muscle cells, H2O2, HOCL

中图分类号: 

  • 中图分类号: R544.1 文献标志码 A 文章编号
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