目的:研究普罗布考(Probucol)和瑞舒伐他汀(Rosuvastatain)对阿霉素诱导心力衰竭大鼠心肌细胞外整合素β1(Integrinβ1)和整合素β3(Integrinβ3)的作用。方法:雄性Wistar大鼠120只,重250±50 g,随机选取15只入空白对照组(Normal组),余105只给予阿霉素诱导心力衰竭。首次给药2个月后存活心衰大鼠随机分成3组:瑞舒伐他汀组(ROS组)、普罗布考组(PRO组)、心衰组(ADR组),将ROS组、PRO组大鼠分别以瑞舒伐他汀,普罗布考进行药物干预,Normal组、ADR组给予蒸馏水灌胃,连续干预4周后处死取材,心脏标本经HE染色、电镜观察大体及超微结构、Masson染色后计算胶原容积分数;免疫组织化学标记左室心肌细胞外整合素β1和β3,应用计算机病理图像分析系统的组化分析模块进行图像分析,计算Integrinβ1及Integrinβ3的相对含量。结果:与ADR组相比,PRO和ROS组大鼠左室胶原容积分数(CVF)显著降低(P<0.05),同时Integrinβ1及Integrinβ3的相对含量显著降低(P<0.05)。结论:PRO及ROS能够显著降低心肌细胞外基质(ECM)Integrinβ1及Integrinβ3的含量,从而明显改善心力衰竭大鼠的左心室功能。 AIM: To investigate the effects of Probucol and rosuvastatain on integrin β1 and integrin β3 in cardiomyocytes induced by doxorubicin in rats with heart failure. Methods: 120 male Wistar rats weighing 250 ± 50 g were randomly selected into the blank control group (Normal group), and the remaining 105 were given doxorubicin to induce heart failure. The surviving heart failure rats were randomly divided into 3 groups: rosuvastatin group (ROS group), probucol group (AD group) and heart failure group (ADR group) after the first administration for 2 months. ROS group, PRO group The rats were treated with rosuvastatin and probucol respectively. Normal group and ADR group were administrated with distilled water. After continuous intervention for 4 weeks, the rats were sacrificed and the heart specimens were observed by HE staining and ultrastructure. Masson staining The volume fraction of collagen was calculated. Immunohistochemistry was used to label the extracellular integrins β1 and β3 in left ventricular myocardium. The histopathological analysis system of the computer was used for image analysis. The relative contents of Integrinβ1 and Integrinβ3 were calculated. Results: Compared with the ADR group, the collagen volume fraction (CVF) of PRO and ROS groups was significantly decreased (P <0.05), while the relative content of Integrinβ1 and Integrinβ3 was significantly decreased (P <0.05). CONCLUSION: PRO and ROS can significantly decrease the content of Integrinβ1 and Integrinβ3 in cardiomyocyte extracellular matrix (ECM), so as to significantly improve left ventricular function in heart failure rats.