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机构地区:[1]辽宁医学院研究生学院,辽宁锦州121001 [2]辽宁医学院附属第一医院特需病房,辽宁锦州121001
出 处:《广东医学》2011年第20期2629-2632,共4页Guangdong Medical Journal
摘 要:目的探讨灯盏花素对糖尿病大鼠心肌转化生长因子-β1(TGF-β1)和Smad7表达的影响。方法健康SD大鼠30只,随机选取20只造模成功后分为糖尿病组(DM组)和灯盏花素治疗组(Bre组)各10只,余10只作为正常对照组(NC组)。Bre组给予灯盏花素注射液20 mg/(kg.d)腹腔内注射,DM组和NC组等量生理盐水腹腔内注射,12周后,尾静脉测血糖,测定大鼠心功能,计算心指数,光镜观察心肌结构病理改变,电镜观察心肌超微结构改变,免疫组化法检测大鼠心肌TGF-β1、Smad7蛋白表达水平。结果 Bre组与DM组间血糖值差异无统计学意义(P>0.05);灯盏花素能显著降低糖尿病大鼠的心指数,明显升高左心室内压最大上升和下降速率,显著减轻心肌病理改变,减少心肌TGF-β1和增加Smad7的表达(P<0.05,P<0.01)。结论灯盏花素可减轻糖尿病大鼠心肌的病理改变,保护糖尿病大鼠心脏功能,其机制可能是通过改善心肌中TGF-β1、Smad7的表达,从而抑制糖尿病大鼠心肌的纤维化来发挥对糖尿病大鼠心脏的保护作用。Objective To observe the effects of breviscapine on the expression of TGF - beta1 and Smad7 in myocardium of diabetic rats. Methods Out of 30 health SD rats, 20 were used for establishment of diabetic rat model and subsequently assigned into DM group and breviscapine treatment group (Bre group). The other 10 rats were used as controis. Intraperitoneal injection of breviscapine parenteral solution [ 20 mg/( kg· d) ] was performed in bre group, while saline substitution was applied in DM and control group. Caudal venous blood glucose measurement, cardiac function, body weight ( BW), heart weight (HW) and HW/BW were assessed in 12th week. The ultrastructural and myocardial structure pathological changes were evaluated by electron microscopy and light microscopy, respectively. The protein levels of TGF - betal and Smad7 were detected by immunohistochemistry. Results There was no significant difference in blood sugar between Bre and DM group ( P 〉 O. 05 ). Reduction of cardiac index, and improvement of maximum velocities of rise and decline of left ventricular pressure were recorded in Bre - treated diabetic rats (P 〈 0. 05 ). Meanwhile, significant al- leviation of myocardial pathological changes, down - regulation of myocardial TGF - betal, and up - regulation of Smad7 were also observed in Bre - treated diabetic rats (P 〈 0. 05). Conclusion Bre viscapine alleviates myocardial pathologi- cal changes and improves cardiac function in diabetic rats, via down - regulation of myocardial TGF - betal and up - regulation of Smad7, thus inhibits diabetic myocardial fibrosis.
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