›› 2010, Vol. 30 ›› Issue (3): 292-.

• 论著(基础研究) • 上一篇    下一篇

缬沙坦对巨噬细胞增殖、炎症因子表达及活性氧生成的抑制作用

纪 艳, 强卫国   

  1. 上海交通大学 医学院瑞金医院 上海市高血压研究所, 上海 200025
  • 出版日期:2010-03-25 发布日期:2010-03-24
  • 通讯作者: 强卫国, 电子信箱: qwg65@126.com。
  • 作者简介:纪 艳(1983—), 女, 硕士生;电子信箱: YANJI200908@yahoo.cn。
  • 基金资助:

    上海市科委基金(034119917)

Inhibition effects of valsartan on cell proliferation, expression of inflammatory factors and reactive oxygen species production of macrophages

JI Yan, QIANG Wei-guo   

  1. Shanghai Institute of Hypertension, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, China
  • Online:2010-03-25 Published:2010-03-24
  • Supported by:

    Shanghai Science and Technology Committee Foundation, 034119917

摘要:

目的 探讨血管紧张素Ⅱ(AngⅡ)受体拮抗剂缬沙坦对巨噬细胞炎症因子表达、活性氧(ROS)生成及其细胞增殖的影响,初步探讨缬沙坦的抗炎作用机制。方法 体外培养小鼠巨噬细胞系RAW264.7并随机分为对照组(10-6 mol/L AngⅡ)和缬沙坦干预组(10-6 mol/L AngⅡ+不同浓度缬沙坦)。Real-time PCR检测肿瘤坏死因子-α(TNF-α)、干扰素诱导蛋白10(IP-10)、白介素-6(IL-6)和巨噬细胞炎性蛋白-2(MIP-2)等炎症因子的表达;荧光探针法检测ROS含量;CCK-8法检测巨噬细胞增殖活性。结果 缬沙坦干预组TNF-α、IP-10、IL-6、MIP-2 mRNA表达均显著低于对照组(P<0.05或P<0.01);不同浓度缬沙坦均能降低细胞ROS含量,其中以10-5 mol/L缬沙坦效果最明显(P<0.05);不同浓度缬沙坦均能降低巨噬细胞的增殖活性(P<0.05或P<0.01),其抑制作用随缬沙坦浓度的上升而更加明显。结论 缬沙坦可能通过抑制巨噬细胞炎症因子表达、ROS生成及细胞增殖而发挥抗炎作用。

关键词: 缬沙坦, 炎症因子, 活性氧, 细胞增殖

Abstract:

Objective To investigate the effects of valsartan, an angiotensinⅡ(AngⅡ)receptor blocker, on expression of inflammatory factors, reactive oxygen species (ROS) production and cell proliferation of macrophages. Methods RAW264.7 macrophages cultured in vitro were randomly divided into control group (10-6 mol/L AngⅡ) and valsartan group (10-6 mol/L AngⅡ+ valsartan). Real-time PCR was used to detect the expression of tumor necrosis factor-α (TNF-α), interferon-inducible protein-10 (IP-10), interleukin-6 (IL-6) and macrophage inflammatory protein-2 (MIP-2), fluorescence probe was employed to determine the ROS production, and CCK-8 was applied to evaluate the cell proliferation of macrophages. Results The expression of TNF-α, IP-10, IL-6 and MIP-2 mRNA in valsartan group was significantly lower than that in control group (P<0.05 or P<0.01). ROS production of macrophages could be inhibited by valsartan, especially by 10-5 mol/L valsartan (P<0.05). Various concentrations of valsartan could decrease proliferation of macrophages in a dose-dependent manner  (P<0.05 or P<0.01). Conclusion The inflammation suppression roles of valsartan may be related with its effects on expression of inflammatory factors, ROS production and proliferation of macrophages.

Key words: valsartan, inflammatory factor, reactive oxygen species, cell proliferation