本文選題：腎素—血管緊張素—醛固酮系統(tǒng) + 肝纖維化�。� 參考：《山東醫(yī)藥》2015年18期

【摘要】：目的觀察阻斷腎素—血管緊張素—醛固酮系統(tǒng)(RAAS)不同環(huán)節(jié)對(duì)實(shí)驗(yàn)性肝纖維化大鼠肝組織纖維化程度的影響并探討其作用機(jī)制。方法取6周齡SD大鼠50只,隨機(jī)分為正常對(duì)照組、模型組、卡托普利組、氯沙坦組和螺內(nèi)酯組各10只。正常對(duì)照組皮下注射橄欖油,其他組給予40%CCL4腹壁皮下注射制備肝纖維化模型;自次日起,卡托普利組、氯沙坦組、螺內(nèi)酯組分別經(jīng)胃管內(nèi)灌注ACE抑制劑卡托普利、血管緊張素(Ang)Ⅱ的Ⅰ型受體阻斷劑氯沙坦、醛固酮受體拮抗劑螺內(nèi)酯,模型組和正常對(duì)照組灌注等量生理鹽水。各組動(dòng)物均于第8周處死,取肝組織行HE染色和Masson染色,觀察其病理變化。ELISA法測(cè)定血清與肝組織中ACE2、AngⅡ、Ang 1-7。結(jié)果卡托普利組、氯沙坦組和螺內(nèi)酯組肝纖維化程度較模型組明顯好轉(zhuǎn);模型組、卡托普利組、氯沙坦組、螺內(nèi)酯組的血清及肝組織中ACE2、AngⅡ、Ang 1-7水平均高于正常對(duì)照組,卡托普利組、氯沙坦組、螺內(nèi)酯組的ACE2及Ang 1-7水平均高于模型組、AngⅡ水平低于模型組(P均0.05);氯沙坦組、螺內(nèi)酯組的ACE2、AngⅡ、Ang 1-7水平與卡托普利組相比差異無統(tǒng)計(jì)學(xué)意義。結(jié)論阻斷RAAS不同環(huán)節(jié)均可抑制肝纖維化形成,其機(jī)制可能是通過升高血清及肝組織中ACE2、Ang 1-7水平、降低AngⅡ水平來發(fā)揮抗肝纖維化的作用。
[Abstract]:Objective to investigate the effects of different links of renin-angiotensin aldosterone system blocking on the degree of hepatic fibrosis in rats with experimental hepatic fibrosis and to explore its mechanism. Methods Fifty SD rats aged 6 weeks were randomly divided into normal control group, model group, captopril group, losartan group and spironolactone group. From the next day, captopril group, losartan group, spironolactone group were intragastrically infused with captopril, ACE inhibitor captopril. Losartan, aldosterone receptor antagonist spironolactone, a type I receptor blocker of angiotensin 鈪，

本文編號(hào)：1793673