哮喘小鼠肺脏组织肾素-血管紧张素系统相关组分表达及AT_1R拮抗剂对其影响  

Expressions of component of renin-angiotensin system in lung tissue of asthmatic mice and effect of AT_1 receptor blocker

作　　者：孙璐瑶[1] 刘颖[1] 于振香[1] 

机构地区：[1]吉林大学第一医院呼吸科,吉林长春130021

出　　处：《吉林大学学报（医学版）》2011年第6期1065-1069,共5页Journal of Jilin University：Medicine Edition

基　　金：吉林省科技厅科研基金资助课题(20110454)

摘　　要：目的:探讨肾素-血管紧张素系统(RAS)与哮喘发生的关系,为哮喘发病机制的研究和治疗提供理论依据。方法:复制小鼠哮喘模型,小鼠分为对照组、模型组、坎地沙坦低剂量组及高剂量组,采集小鼠血清,测量血清中血管紧张素Ⅱ(AngⅡ)与血管紧张素Ⅰ(AngⅠ)的含量;通过Western blotting和RT-PCR观察RAS中血管紧张素原(AGT)、血管紧张素转换酶(ACE)、血管紧张素Ⅱ1型受体(AT1R)和2型受体(AT2R)在各组小鼠肺组织中的表达。结果:模型组小鼠血清AngⅡ含量较对照组增高(P<0.05),坎地沙坦组与模型组比较无明显变化(P>0.05)。各组小鼠血清中AngⅠ含量比较差异无统计学意义(P>0.05)。模型组小鼠AT1R和ACE蛋白表达较对照组明显增加(P<0.05),坎地沙坦组AT1R表达与模型组比较明显降低(P<0.05),ACE无明显变化(P>0.05)。AT2R蛋白表达各组间比较差异无统计学意义(P>0.05)。模型组小鼠ACE mRNA表达较对照组明显增加(P<0.05),坎地沙坦组与模型组比较差异无统计学意义(P>0.05)。模型组小鼠AT1R mRNA表达较对照组明显增加(P<0.05),坎地沙坦组较模型组明显降低(P<0.05)。模型组AT2R mRNA较对照组明显降低(P<0.05),坎地沙坦组较模型组明显增加(P<0.05)。各组AGT mRNA表达无明显变化(P>0.05)。结论:在小鼠哮喘发病过程中,RAS活化参与了哮喘的发病过程,并且AT1R拮抗剂坎地沙坦可以逆转ACE、AT1R和AT2R表达的改变。Objective To investigate the relationship between the renin-angiotensin system(RAS)and asthma,and provide the theoretical basis for pathogenesis and treatment of asthma.Methods The mouse asthma models were set up and divided into control group,model group,candesartan low-dose group,and candesartan high-dose group.The serum of mice was collected,the levels of serum angiotensin Ⅱ(AngⅡ) and angiotensin Ⅰ(AngⅠ) were detected;the changes of angiotensinogen(AGT),angiotensin-convertion enzyme(ACE),angiotensin Ⅱ type 1 receptor(AT1R) and angiotensin Ⅱ type 2 receptor(AT2R) in the RAS of the mouse lung tissue were delected by Western blotting and RT-PCR.Results The serum Ang Ⅱ level in model group was higher than that in control group(P<0.05),but the level of AngⅡ in candesartan groups had no significant changes compared with model group(P>0.05).The serum Ang Ⅰlevels in each group had no significant changes(P>0.05).The expressions of AT1R and ACE protein in model group were markedly increased compared with control group(P<0.05),the AT1R expressions in candesartan groups were significantly decreased compared with model group(P<0.05),but ACE unchanged.There were no significant differences of the expressions of AT2R protein between various groups(P>0.05).The ACE mRNA expression in model group was increased significantly compared with control group(P<0.05),but there was no significant change in candesartan groups compared with model group(P>0.05).The AT1R mRNA expression in model group was significantly increased compared with control group(P<0.05),the AT1R expressions in candesartan groups were significantly reduced compared with model group(P<0.05).The AT2R mRNA in model group was significantly decreased compared with model group(P<0.05),the expressions in candesartan groups were significantly increased compared with model group(P<0.05).The expression of AGT mRNA in each group had no significant change.Conclusion In the course of asthma of mice,RAS activation is involved in the pathogenesis of asthma,and t

关 键 词：哮喘 肾素-血管紧张素系统 血管紧张素Ⅱ1型受体拮抗剂 

分 类 号：R56[医药卫生—呼吸系统]