| 注册
首页|期刊导航|基础医学与临床|巨噬细胞增强H2O2抑制人血管内皮细胞和兔血管平滑肌细胞的增殖

巨噬细胞增强H2O2抑制人血管内皮细胞和兔血管平滑肌细胞的增殖

李天佳 刘暴 倪冷 来志超 吴立飞 刘昌伟

基础医学与临床2013,Vol.33Issue(7):849-853,5.
基础医学与临床2013,Vol.33Issue(7):849-853,5.

巨噬细胞增强H2O2抑制人血管内皮细胞和兔血管平滑肌细胞的增殖

Macrophages enhance the inhibition of H2O2 on the proliferation of human vascular endothelial cells and rabbit smooth muscle cells

李天佳 1刘暴 1倪冷 1来志超 1吴立飞 1刘昌伟1

作者信息

  • 1. 中国医学科学院北京协和医学院北京协和医院血管外科,北京100005
  • 折叠

摘要

Abstract

Objective Investigate the changes of inflammatory factors secreted by macrophages exposed to oxidative stress,and their effect on the proliferation of vascular endothelial cells and smooth muscle cells.Methods The groups described as followings:control,macrophage,0.5 mmol/L H2O2,macrophage + 0.5 mmol/L H2O2.The growth curves of VECs and VSMCs under different conditions were measured by CCK-8.The IL-6,IL-10,MCP-1,TNF-αt and VEGF were detected by ELISA.The level of PCNA,cyclinD1 and eNOS were analysised by Western blot.Results The proliferation of control group was higher than the others in VEC (P < 0.05),while in VSMC,the proliferation of control group was lower than that of macrophage group (P < 0.05).In both VEC and VSMC,macrophages + 0.5 mmol/L H2O2 conditioned medium groups were higher than 0.5 mmol/L H2O2 groups (P <0.05),while were lower than macrophage groups (P <0.05).The secretions of IL-6,IL-10,and MCP-1 in macrophages were increased with time and H2O2 concentration(P <0.05),while the titer of TNF-α didn't change significantly.Only the concentration of H2O2 reached 1.0 mmoL/L,and secretion of VEGF increased significantly (P < 0.05).Conclusions The oxidative stress affect the secretions of inflammatory cytokines secreted by macrophages,and thus regulate proliferations of vascular endothelial cells and smooth muscle cells.

关键词

氧化应激/炎性因子/增殖

Key words

oxidative stress/ inflammatory factors/ proliferation

分类

医药卫生

引用本文复制引用

李天佳,刘暴,倪冷,来志超,吴立飞,刘昌伟..巨噬细胞增强H2O2抑制人血管内皮细胞和兔血管平滑肌细胞的增殖[J].基础医学与临床,2013,33(7):849-853,5.

基金项目

北京市自然科学基金(7122145) (7122145)

基础医学与临床

OA北大核心CSCDCSTPCD

1001-6325

访问量0
|
下载量0
段落导航相关论文