Exercise has an effect on the reduction of myocardial fibrosis in diabetic rats as previously reported, in which oxidative stress and the TGF-β1/Smad signaling pathway may play key roles. There is little direct experimental evidence that exercise alleviates myocardial fibrosis in type 2 diabetes mellitus (T2DM). Here we established a type 2 diabetic model by using streptozotocin and a high-fat diet. Rats were divided into groups of normal control (NC), T2DM and T2DM plus exercise (T2DME). The T2DME group received further treadmill training at moderate intensity for 8 weeks. Histological and biochemical methods were used to detect the benefits of exercise to T2DM. Results showed that the weight of rats in the T2DM group dropped dramatically, along with significant increases in blood glucose, myocardial fibrosis and oxidative stress, associated with upregulated expression of factors of myocardial fibrosis, except Smad7. Exercise largely reversed T2DM-induced alterations in factors of myocardial fibrosis, including suppressing expression of MMP-2, CTGF, TGF-β1, p-Smad2 and p-Smad3, and increased expression of TIMP-1 and Smad7. Therefore, exercise might be considered an alternative therapeutic remedy for diabetic cardiomyopathy.

中文翻译：

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长期中等强度运动通过抑制氧化应激和TGF-β1/Smad通路减轻2型糖尿病大鼠心肌纤维化。


正如之前报道的，运动可以减少糖尿病大鼠的心肌纤维化，其中氧化应激和TGF-β1/Smad信号通路可能发挥关键作用。几乎没有直接的实验证据表明运动可以减轻 2 型糖尿病 (T2DM) 的心肌纤维化。在这里，我们通过使用链脲佐菌素和高脂肪饮食建立了 2 型糖尿病模型。将大鼠分为正常对照组（NC）、T2DM 组和 T2DM 加运动组（T2DME）。 T2DME组进一步接受中等强度的跑步机训练，为期8周。采用组织学和生化方法检测运动对 T2DM 的益处。结果显示，T2DM组大鼠体重急剧下降，血糖、心肌纤维化和氧化应激显着升高，这与除Smad7外的心肌纤维化因子表达上调有关。运动在很大程度上逆转了 T2DM 诱导的心肌纤维化因子的改变，包括抑制 MMP-2、CTGF、TGF-β1、p-Smad2 和 p-Smad3 的表达，以及增加 TIMP-1 和 Smad7 的表达。因此，运动可能被认为是糖尿病心肌病的替代治疗方法。