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机构地区:[1]郑州大学第二附属医院心内科,郑州市450014
出 处:《医药论坛杂志》2006年第24期7-9,共3页Journal of Medical Forum
摘 要:目的探讨结缔组织生长因子(CTGF)在慢性心衰大鼠心肌纤维化(myocard ial fibrosis,MF)发生发展中的作用,以及辛伐他汀改善慢性心衰时心室重构和MF可能的作用机制。方法30只雄性W istar大鼠随机分为三组,假手术组(sham组)8只,模型组(model组)及辛伐他汀组(simvastatin组),每组11只。采用腹主动脉缩窄法制作慢性心衰模型,喂养8周后simvastatin组大鼠予以辛伐他汀2mg/(kg.d)灌胃,model组用生理盐水灌胃。8周后检测血流动力学参数,用MASSON染色法观察左室心肌胶原形态,图像分析测量胶原容积分数(CVF)和血管周围胶原面积(PVCA),免疫组化法检测心室肌中TGF-β1、CTGF表达。结果①CVF、PVCA在model组大鼠明显高于sham组大鼠(P<0.01);与model组比较,simvastatin组则显著降低(P<0.01)。②TGF-β1、CTGF在sham组表达较弱,model组表达增强,simvastatin组则减弱。结论辛伐他汀明显改善心室重构和MF,改善心功能,此作用可能与影响CTGF表达有关。Objective To investigate the role of connective tissue growth factor (CTGF) in development of myocardial fibrosis (MF) in rats with chronic heart failure, and the mechanism of simvastatin to attentuate myocardial remodeling and myocardial fibrosis in rats with chronic heart failure. Methods 30 male Wistar rats were randomly assigned to sham -operated group ( n = 8 ), model group( n = 11 )and simvastatin group( n = 11 ). The animal model was established by suprarenal aortic constriction. After 8 weeks common fed, rats in simvastatin group were given a daily dose of 2 mg/( kg · d) of simvastatin for 8 weeks by gastric lavage and the other two groups were fed with normal saline. Hemodynamic parameters of 3 groups rats were detected, expressions of TGF -β1 ,CTGF in myocardium were evaluated by qualitative and semiquantitative immunohistochemical staining. MASSON staining was used in the study of total Collagen type in left ventricular interstitial tissue. Collagen volume fraction (CVF) , Perivascular collagen area (PVCA) were measured by image analysis. Results Compared with the sham - group, CVF, PVCA, and the expression of TGF - β1, Connective tissue growth factor in left ventricle increased in model group ( P 〈 0. 01 ). Compared with the model group rats ,these indexes decreased in simvastatin group obviously. ( P 〈 0. 01 ). Conclusion Simvastatin obviously attentuates myocardial remodeling and myocardial fibrosis of rats with chronic heart failure, improves cardiac function ,which is dependent on its effect on expressions of TGF- β1 and Connective tissue growth factor.
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