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目的通过研究红芪多糖(HPS)对db/db小鼠糖尿病心肌病(DCM)心肌组织中TGF-β1/Smads信号通路的影响,探讨其对DCM小鼠心肌纤维化的影响。方法将60只6周龄雄性db/db小鼠随机分为5组:HPS高、中、低剂量组,罗格列酮组和模型组;正常组为12只同周龄同背景的非转基因雄性db/m小鼠。连续灌胃干预8周。于给药前及给药后第2、4、6、8周末检测各组小鼠体重、血糖;HE染色观察小鼠左心室心肌纤维病理形态学变化;Masson染色观察小鼠左心室心肌胶原纤维化程度;Western blot、RT-PCR法检测心肌组织TGF-β_1及Smad2、Smad3蛋白和mRNA的表达。结果经HPS治疗8周后,HPS高、中剂量组和罗格列酮组血糖较模型组下降明显(P<0.05);HE染色可见模型组心肌细胞结构模糊,部分区域明显肿胀变形且细胞核消失;Masson染色可见亮绿色胶原纤维在模型组心肌细胞间及血管周围较正常组明显增多且呈堆积状分布;模型组TGF-β_1及Smad2、Smad3蛋白及mRNA的表达水平与HPS低剂量组无显著差异(P>0.05),其余各治疗组较模型组明显降低(P<0.05),其中HPS高剂量组和罗格列酮组改善更明显(P<0.05)。结论 HPS可改善db/db小鼠DCM心肌纤维化的程度,延缓DCM病情进展,其作用机制可能与其抑制TGF-β_1/Smads信号通路有关。
Objective To investigate the effect of Hedysarum polysaccharide (HPS) on TGF-β1 / Smads signal pathway in db / db mice with diabetic cardiomyopathy (DCM) and to investigate its effect on myocardial fibrosis in DCM mice. Methods Sixty six 6-week-old male db / db mice were randomly divided into 5 groups: HPS high, medium and low dose groups, rosiglitazone group and model group. In the normal group, 12 non-transgenic Male db / m mice. Continuous gavage intervention for 8 weeks. The body weight and blood glucose of the mice in each group were measured before treatment and at the end of the 2nd, 4th, 6th and 8th weeks after administration. Pathological changes of left ventricular myocytes were observed by HE staining. Masson staining was used to observe the changes of left ventricular myocardial collagen fibers The expression of TGF-β 1, Smad2 and Smad3 protein and mRNA in myocardium were detected by Western blot and RT-PCR. Results After HPS treatment for 8 weeks, the blood glucose of HPS high, middle dose and rosiglitazone groups was significantly lower than that of the model group (P <0.05). HE staining showed that the myocardial cells in the model group were vaguely swollen and some of them were swollen and deformed and the nuclei disappeared ; Masson staining showed bright green collagen fibers in the model group of myocardial cells and perivascular than the normal group was significantly increased and the accumulation of distribution; model group TGF-β 1 and Smad2, Smad3 protein and mRNA expression levels and HPS low dose group was not significant (P> 0.05). The rest of the treatment groups were significantly lower than the model group (P <0.05), of which HPS high dose group and rosiglitazone group improved more significantly (P <0.05). Conclusion HPS can improve the degree of myocardial fibrosis in DCM and delay the progression of DCM, which may be related to the inhibition of TGF-β 1 / Smads signaling pathway.