巨噬细胞极化在缺氧性肺动脉高压中的作用  

The role of macrophage polarization in hypoxic pulmonary hypertension

作　　者：孙得胜 刘虹延[3] 罗志梅 欧阳瑶 刘先胜 SUN De-Sheng;LIU Hong-Yan;LUO Zhi-Mei(Department of Respiratory and Critical Care Medicine,Affiliated Hospital of Zunyi Medical University,Zunyi 563003,Guizhou,China)

机构地区：[1]遵义医科大学附属医院呼吸与危重症医学科,贵州遵义563003 [2]华中科技大学同济医学院附属同济医院呼吸与危重症医学科,国家卫健委呼吸疾病重点实验室 [3]遵义医科大学附属医院针灸科

出　　处：《中国老年学杂志》2024年第2期360-363,共4页Chinese Journal of Gerontology

基　　金：国家自然科学基金(82260014,81960016);遵义医科大学博士科研启动资金项目(院字(2018)04号)。

摘　　要：目的观察缺氧性肺动脉高压大鼠肺组织中CD68、Arg1、诱导型一氧化氮合酶(iNOS)表达变化,探讨缺氧性肺动脉高压与巨噬细胞极化的关系。方法20只清洁级SD大鼠,采用随机数字表法分为对照组和模型组,各10只,模型组在实验动物缺氧装置中给予常压缺氧(10%O 2),每天缺氧8 h,同时给予充足的饮食,持续4 w。对照组不予以低氧刺激。28 d后在生理多导仪监视下,通过右心漂浮导管测定两组右心室收缩压力,判断造模是否成功。测压后以免疫组织化学法观察肺组织和肺血管中CD68、Arg1、iNOS表达和分布。结果与对照组相比,模型组右心室收缩压显著升高(P<0.05),缺氧性肺动脉高压模型建立成功。与对照组比较,模型组巨噬细胞标志物CD68、M2型巨噬细胞标志物Arg1表达明显升高,M1型巨噬细胞标志物iNOS表达明显降低(均P<0.05)。结论巨噬细胞可能参与了缺氧性肺动脉高压的发病,且巨噬细胞向M2方向的极化可能在这一过程中发挥了作用。Objective To observe the changes in the expressions of CD68,Arg1 and inducible nitric oxide synthase(iNOS)in the lung tissues of rats with hypoxic pulmonary hypertension,and to investigate the relationship between hypoxic pulmonary hypertension and macrophage polarization.Methods Twenty clean SD rats were randomly divided into control group and model group,with 10 rats in each group.The model group was given atmospheric hypoxia(10%O 2)for 8 h a day and adequate diet for 4 w in a hypoxia apparatus for experimental animals.The control group did not receive hypoxic stimulation.After 28 d,the right ventricular systolic pressure of rats in both groups was measured by right heart floating catheter under the monitoring of physiological multichannel instrument,and the success of modeling was judged.After pressure measurement,the expression and distribution of CD68,Arg1 and iNOS in lung tissues and pulmonary blood vessels were observed by immunohistochemistry.Results Compared with the control group,the right ventricular systolic pressure in the model group was significantly increased(P<0.05),which implied the successful construction of the model of hypoxic pulmonary hypertension.Compared with the control group,the expressions of the macrophage marker CD68 and M2-type macrophage marker Arg1 were significantly improved,the expression of M1-type macrophage marker iNOS was significantly reduced(all P<0.05).Conclusions Macrophages might be involved in the pathogenesis of hypoxic pulmonary hypertension,and macrophage polarization toward M2 might play a role in this pathogenesis.

关 键 词：巨噬细胞 极化 缺氧 肺动脉高压 

分 类 号：R544[医药卫生—心血管疾病]