【摘要】 目的探讨卡托普利对大鼠肝纤维化的治疗作用及其机制。方法采用四氯化碳(CCl4)制造大鼠肝纤维化模型,设正常组、模型组、卡托普利低剂量组和卡托普利高剂量组,采用放射免疫法测定血液和肝匀浆中肾素活性、血管紧张素和醛固酮;采用紫外分光光度法测定血管紧张素转换酶活性;图像分析法判定肝纤维化程度。结果卡托普利能降低肝内肾素-血管紧张素-醛固酮系统(RAAS)活性(P<0.01),减轻肝纤维化(P<0.01),两剂量之间差异无显著性。结论卡托普利具有抗肝纤维化作用;其机制可能是抑制肝内RAAS激活。更多还原

【Abstract】 【Objective】 To investigate the effects of Captopril on rat hepatic fibrosis and explore the underlying mechanism.【Methods】 Forty healthy SD rats were randomly divided into four groups: normal control group,model group,Captopril low dosage group,Captopril high dosage group.Liver and plasma renin activity,angiotensin I& 11,and aldosterone were detected by radio-immunoassay.Angiotensin converting enzyme activity was detected by ultra-violet spectrophotography.The area of collagen was examined by the image analysis system.【Results】 Captopril could inhibit the liver rennin-angiotensin-aldosterone system(P <0.01),and ameliorate liver fibrosis(P <0.01).There was no difference between two dosage groups.【Conclusion】 Captopril could attenuate rat liver fibrogenesis by inhibiting the activity of the liver rennin-angiotensin-aldosterone system.更多还原