卡托普利对肝纤维化大鼠转化生长因子β1及血小板源性生长因子-BB的影响  

Influence of Captopril on TGFβ_1 and PDGF-BB in hepatic fibrosis rats

作　　者：鲁福德[1] 严永杰[1] 林春英[1] 

机构地区：[1]广州医学院从化学院,广东广州510925

出　　处：《现代中西医结合杂志》2005年第23期3060-3061,共2页Modern Journal of Integrated Traditional Chinese and Western Medicine

摘　　要：目的观察卡托普利抗大鼠肝纤维化的疗效。方法60只Wistar大鼠随机平均分为3组:正常组、模型组和治疗组。四氯化碳(CCl4)诱导大鼠肝纤维化模型,治疗组于造模第4周开始予以卡托普利。免疫组化法检测大鼠肝组织中转化生长因子β1(TGFβ1)、血小板源性生长因子-BB(PDGF-BB);肝组织HE染色检测病理改变。结果与模型组大鼠比较,治疗组TGFβ1与PDGF-BB在肝组织表达明显降低;卡托普利治疗后肝小叶均趋于正常,纤维间隔明显变薄。结论卡托普利能有效地减轻肝纤维化大鼠的肝脏损伤及纤维化程度,其机制可能与直接或间接抑制TGFβ1与PDGF-BB生成有关。Objective It is to observe the curative effect of Captopril on hepatic fibrosis rats. Methods 60 Wistar rats were randomly divided into normal group, model group and treatment group. Hepatic fibrosis model rats were induced with CCl4. Treatment group were given Captopril at the fourth week after the model induced. Transforming growth factor β1 （TGFβ1 ） and platelet-derived growth factor （PDGF） - BB in rats＇ hepatic tissue were detected with immunohistochemical, The hepatic tissue patho-change was detected with HE staining. Results Compared with model group, the expressions of TGFβ1 and PDGF- BB in hepatic tissue in treatment group were obviously debased （P 〈 0.05 ）. The hepatic lobules were all incline to normal and the tissue intervals were all obviously thinned. Conclusion Captopril can effectively lighten liver injury and hepatic fibrosis degree. Its mechanism may be related to its inhibiting TGFβ1 and PDGF - BB producing directly and indirectly.

关 键 词：血管紧张素转换酶抑制荆 肝纤维化 转化生长因子Β1 血小板源性生长因子-BB 

分 类 号：R-332[医药卫生]