红芪多糖对模型小鼠糖尿病心肌病心肌纤维化和基质金属蛋白酶2及其抑制剂表达影响.docVIP

红芪多糖对模型小鼠糖尿病心肌病心肌纤维化和基质金属蛋白酶2及其抑制剂表达影响 　　摘要：目的 观察红芪多糖（HPS）对模型小鼠心肌组织基质金属蛋白酶2（MMP-2）及其抑制剂（TIMP-2）表达的影响，探讨其防治糖尿病心肌病心肌纤维化的作用机制。方法 将60只实验小鼠随机分为模型组、罗格列酮组和HPS高、中、低剂量组，正常组为12只同周龄同背景的非转基因雄性BKS.Cg-Dock7m+/+Leprdb/JNju小鼠。各?M给予相应药物灌胃，连续8周。给药前及给药2、4、6、8周末检测小鼠血糖；Masson染色观察心肌纤维化程度；蛋白印迹法检测心肌组织MMP-2、TIMP-2的蛋白表达。结果 与模型组比较，HPS高、中剂量组和罗格列酮组小鼠血糖明显下降。Masson染色结果显示，模型组小鼠心肌间质中亮绿色纤维较正常组明显增多，HPS高剂量组、罗格列酮组较模型组有所减少。蛋白质印迹检测结果显示，与正常组比较，模型组小鼠MMP-2表达明显降低，TIMP-2表达明显升高，MMP-2/TIMP-2比值下降；与模型组比较，HPS高、中剂量组和罗格列酮组小鼠MMP-2表达明显升高，TIMP-2表达明显降低，MMP-2/TIMP-2比值上升。结论 HPS可减轻模型小鼠糖尿病心肌病心肌纤维化程度，其治疗作用可能是通过升高MMP-2/TIMP-2比值，从而使模型小鼠心肌纤维化有所减轻。 　　关键词：糖尿病心肌病；红芪多糖；基质金属蛋白酶-2；基质金属蛋白酶组织抑制因子-2；小鼠 　　DOI：10.3969/j.issn.1005-5304.2017.04.015 　　中图分类号：R285.5 文献标识码：A 文章编号：1005-5304（2017）04-0057-04 　　Effects of HPS on Myocardial Fibrosis and Expression of MMP-2/TIMP-2 in Model Mice of Diabetic Cardiomyopathy WANG Dong-xv， JIN Zhi-sheng， ZHANG Hua-zhi， HE Cai-ling， NAN Xiang-ping， SHI Gui-zhen， CHU Hui-yuan （Gansu University of Chinese Medicine， Lanzhou 730000， China） 　　Abstract： Objective To observe the effects of hedysari polysaccharide （HPS） on myocardial fibrosis and the expression of MMP-2/TIMP-2 in model mice of diabetic cardiomyopathy； To discuss the mechanism of action of prevention and treatment of myocardial fibrosis in diabetes. Methods Sixty mice were randomly divided into model group， rosiglitazone group and HPS high-， mediume- and low-dose groups. The normal group was 12 non-transgenic male BKS.Cg-Dock7m+/+Leprdb/JNju mice with the same age. Each group was given relevant medicine for gavage， for 8 weeks. Blood glucose of mice before and after medication 2， 4， 6， and 8 weeks was detected. The levels of MMP-2， MMP-2 and MMP-9 in myocardium were measured by Masson staining. The protein expressions of MMP-2 and TIMP-1 in myocardium were detected by Western blot. Results Compared with the model group， the blood glucose of HPS （high- and medium dose） groups and rosiglitazone group decreased significantly. Masson staining sh