ACE及ACE2在慢性香烟烟雾诱导的大鼠肺动脉高压对血管紧张素Ⅱ的调控作用  

Effect of ACE and ACE2 on cigarette smoke-induced pulmonary hypertension in rat lungs

作　　者：韩素霞[1] 周彦梅[1] 郭李平[1] 常建梅[1] 徐洁[1] 冯磊[1] 

机构地区：[1]新疆医科大学第五附属医院心血管内科,乌鲁木齐市830000

出　　处：《中国心血管病研究》2014年第4期330-333,383,共5页Chinese Journal of Cardiovascular Research

基　　金：国家自然科学基金项目（项目编号：81060023）

摘　　要：目的 探讨慢性香烟暴露诱导的肺动脉高压形成过程中ACE、ACE2和血管紧张素Ⅱ（AngⅡ）的调控作用及特异性血管紧张素Ⅱ受体拮抗剂氯沙坦的治疗作用.方法 健康雄性SD大鼠60只,随机分为A组：对照组（Con）;B组：30 mg/kg单纯氯沙坦组（30 mg/kg Los）;C组：香烟诱导组（SM）;D组：香烟诱导＋10 mg/kg氯沙坦组（SM＋10 mg/kg Los）;E组：香烟诱导＋30 mg/kg氯沙坦组（SM＋30 mg/kg Los）.香烟暴露组和香烟暴露＋氯沙坦组在标准毒理香烟暴露箱中接受被动吸烟;对照组同时在同种毒理箱中暴露于新鲜空气;氯沙坦给药采用每天腹腔内注射;正常对照组给予等量生理盐水注射.建立香烟诱导的肺动脉高压大鼠模型后,用插入导管法检测右室收缩压（RVSP）;Western blotting法分析ACE2和ACE的蛋白表达量;放射免疫分析试剂药盒测定肺组织中的AngⅡ表达水平.结果 香烟暴露6个月后,慢性香烟暴露组大鼠RVSP较对照组明显升高,大鼠肺组织中AngⅡ表达水平显著增高.Western blotting结果显示,ACE表达水平增高,香烟暴露组大鼠肺组织ACE2蛋白表达水平降低,而ACE蛋白表达水平较对照组升高.氯沙坦干预治疗后,香烟暴露＋氯沙坦组大鼠RVSP和AngⅡ较香烟暴露组降低（P＜0.05）,肺组织ACE2蛋白表达水平较香烟暴露组增强,ACE蛋白表达水平较香烟暴露组减少（P＜0.05）.结论 慢性香烟暴露可导致肺动脉高压,还可刺激肺组织ACE2和ACE的蛋白表达变化,提示ACE2和ACE在慢性香烟暴露诱导的肺动脉高压中起一定作用.Objective Cigarette smoking may induce pulmonary hypertension.The potential role of ACE2 and ACE in cigarette smoke-induced is yet unclear.Methods Rata were randomly divided into five groups：A：control,B：control plus losartan,C：smoke exposure only,D：smoke exposure plus＋10 mg/kg losartan,E：smoke exposure plus＋30 mg/kg losartan.The C and D groups were exposed to the smoke of 15 commercial cigarettes.After 6 months,right ventricle systolic pressure（RVSP）,biochemical changes were examined.Results The RVSP and Ang Ⅱ were raised and the level of lung tissue ACE2 was decreased in cigarette smoke-induced pulmonary hypertension in rata compared with that in control group.The RVSP and Ang Ⅱ were reduced and ACE2 was increased as shown by inhibition with losartan.Conclusion This study demonstrated that ACE2 and ACE played an essential role in smoke-induced pulmonary hypertension.

关 键 词：香烟 肺动脉高压 血管紧张素转换酶 血管紧张素转换酶2 氯沙坦 

分 类 号：Q95-33[生物学—动物学] R543.2[医药卫生—心血管疾病]