期刊文献+

替米沙坦对小鼠巨噬细胞M1/M2亚型极化的影响 被引量:5

Effect of Telmisartan on mice macrophage M1/M2 polarization
下载PDF
导出
摘要 目的探讨替米沙坦对小鼠巨噬细胞M1/M2亚型极化的影响。方法分别用脂多糖(LPS)联合干扰素-γ(IFN-γ)和白介素-4(IL-4)诱导小鼠巨噬细胞M1/M2型极化,用免疫荧光法检测极化结果。在M1型巨噬细胞中分别加入0.1、1、10μmol/L替米沙坦,同时设立空白对照组及溶剂对照组,Western blot法检测各组巨噬细胞亚型标志物诱导性一氧化氮合酶(iN OS)和精氨酸酶Ⅰ(ArgⅠ)的表达情况,ELISA法检测各组培养液上清中IL-6、IL-10表达情况。结果在LPS+IFN-γ诱导的小鼠巨噬细胞中M1型巨噬细胞标志物iN OS、IL-6的表达水平明显升高,替米沙坦干预后,各干预组M1型巨噬细胞标志物iN OS、IL-6的表达水平下降(P<0.05),随着替米沙坦浓度的增加而降低,而代表M2型巨噬细胞标志物的ArgⅠ和IL-10表达水平上升(P<0.05)。结论替米沙坦可以抑制LPS+IFN-γ诱导的小鼠巨噬细胞M1型极化,促进M1型巨噬细胞向M2型巨噬细胞转化。 Objective To investigate the effect of Telmisartan on the M1/M2 polarization of mice macrophage.Methods Mice macrophage was induced to M1/M2 polarization by LPS+IFN-γ and IL-4 respectively,and tested by immunofluorescence. Meanwhile cells were treated with 0. 1,1,10 μmol / L Telmisartan,blank control group and vehicle control group were established at the same time. The biomarkers i NOS and Arg Ⅰ were tested by Western blot,and the cytokines IL-6 and IL-10 were tested by ELISA assay. Results The biomarker i NOS and IL-6,secreted by M1 macrophage,were apparently increased in the macrophages induced by LPS + IFN-γ. However,after being treated with Telmisartan,the expressions of i NOS and IL-6 were obviously decreased( P〈0. 05),as the concentration higher the expression lower. While,the expression of Arg I and IL-10,which represented the M2 macrophage,increased( P〈0. 05). Conclusion Telmisartan can inhibit the M1 polarization of mice macrophage RAW264. 7 induced by LPS and IFN-γ and transform M1 macrophage polarization to M2 macrophage polarization.
出处 《安徽医科大学学报》 CAS 北大核心 2016年第7期989-992,997,共5页 Acta Universitatis Medicinalis Anhui
基金 高等学校博士学科点专项科研基金(编号:20123420120005) 安徽高校省级自然科学研究重点项目(编号:KJ2012A147)
关键词 替米沙坦 巨噬细胞M1/M2型极化 炎症 Telmisartan macrophage M1/M2 polarization inflammation
  • 相关文献

参考文献11

  • 1Hu Z P, Wang B N, Qian H Y, et al. Fixed-dose telmisartan/ hydrochlorothiazide in comparison with losartmr/hydrochlorothiaz- ide in decreasing serum hepatocyte growth factor and improving en- dothelial dysfunction in hypertensive patients [ J ]. Int Heart J, 2010,51 (4) :252 -8. S.
  • 2loop G D. Atherosclerosis -an inflammatory disease[ J ]. N Engl J Med, 1999, 340(24) :1928.
  • 3Colin S, Chinetti-Gbaguidi G, Staels B. Macrophage phenotypes in atherosclerosis[ J]. Inmmnol Rev, 2014, 262 ( 1 ) : 153 - 66.
  • 4Libby P, Ridker P M, Hansson G K. Inflammation in atheroscle- rosis: from pathophysiology to practice [ J ]. J Am Coil Cardiol, 2009, 54(23) :2129 -38.
  • 5van Tits L J, Stienstra R, van Lent P L, et al. Oxidized LDL en- hances pro-inflammatory responses of alternatively activated M2 macrophages : a crucial role for Krtippel-like factor 2 [ J ]. Athero- sclerosis, 2011, 214(2):345-9.
  • 6Lee C W, Hwang I, Park C S, et al. Macrophage heterogeneity of culprit coronary plaques in patients with acute myocardial infarc-tion or stable angina[J]. Am J Clin Pathol, 2013, 139(3) :317- 22.
  • 7Stager J L, Gijbels M J, van der Velden S, et al. Distribution of macrophage polarizationmarkers in human atherosclerosis [ J ]. Ath- erosclerosis ,2012,225 (2) :461 - 8.
  • 8Federica D P, Bart S, Giulia C G. Macrophage phenotypes and their modulation in atherosclerosis [ J ]. Circ J, 2014, 78 ( 8 ) : 1775 - 81.
  • 9Babaev V R,Yancey P G,Ryzhov S V,et al. Conditional knockout of macrophage PPARgamma increases atherosclerosis in C57BL/6 and low-density lipoprotein receptor-deficient mice [ J ]. Arterioscler Thromb Vasc Biol,2005,25:1647 -53.
  • 10E1 Hadri K, Mahmood D F, Couchie D, et al. Thioredoxin-1 pro- motes anti-inflammatory macrophages of the M2 phenotype and an- tagonizes atherosclerosis[ J]. Arterioscler Thromb Vasc Biol,2012, 32(6) :1445 -52.

同被引文献42

引证文献5

二级引证文献23

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部