Stem cell (SC) therapy is a promising approach to improve post-myocardial infarction (MI) cardiac remodeling, but the proinflammatory microenvironment may lead to SC loss and, therefore, may have a negative impact on therapy. It appears that exercise training (ET) improves myocardial microenvironment for SC transplantation. Therefore, we tested the effect of ET on post-infarction retention of adipose-derived SCs (ADSCs) and its combined effects on the inflammatory microenvironment. Fischer-344 female rats were randomized to one of the following groups: Sham; sedentary coronary occlusion who did not receive ADSCs (sMI); sedentary coronary occlusion who received ADSCs; exercise coronary occlusion who received ADSCs. Rats were trained nine weeks prior to MI, followed by ADSCs transplantation. The MI led to left ventricle (LV) dilation and dysfunction, myocardial hypertrophy and fibrosis, and increased proinflammatory profile compared to Sham rats. Conversely, ADSCs transplanted rats exhibited, better morphological and functional LV parameters; inhibition of myocardial hypertrophy and fibrosis; and attenuation of proinflammatory cytokines (interleukins 1β and 10, tumor necrosis factor α, and transforming growth factor β) in the myocardium compared to sMI rats. Interestingly, ET enhanced the effect of ADSCs on interleukin 10 expression. There was a correlation between cytokine expression and myocardial ADSCs retention. The. ET enhanced the beneficial effects of ADSCs in infarcted myocardium, which was associated with higher ADSCs retention. These findings highlight the importance of ET in myocardial retention of ADSCs and attenuation of cardiac remodeling post-infarction. Cytokine analysis suggests improvement in ET-linked myocardial microenvironment based on its anti-inflammatory action.

中文翻译：

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通过锻炼前训练，增加心肌梗死后间充质干细胞的心肌保留。

干细胞（SC）治疗是改善心肌梗死后（MI）心脏重塑的一种有前途的方法，但促炎性微环境可能导致SC丢失，因此可能对治疗产生负面影响。看来运动训练（ET）可以改善SC移植的心肌微环境。因此，我们测试了ET对脂肪来源的SC（ADSC）在梗死后保留的作用及其对炎症微环境的综合作用。将Fischer-344雌性大鼠随机分为以下一组：Sham；久坐不接受ADSC（sMI）的冠状动脉闭塞；久坐的接受ADSC的冠状动脉闭塞；运动接受ADSC的冠状动脉闭塞。在MI发生前9周对大鼠进行训练，然后进行ADSC移植。MI导致左心室（LV）扩张和功能障碍，与假手术大鼠相比，心肌肥大和纤维化，以及促炎特征增加。相反，ADSCs移植大鼠表现出更好的形态学和功能性LV参数。抑制心肌肥大和纤维化；与sMI大鼠相比，心肌中促炎细胞因子（白介素1β和10，肿瘤坏死因子α和转化生长因子β）的抑制和减弱。有趣的是，ET增强了ADSC对白介素10表达的影响。细胞因子表达与心肌ADSCs保留之间存在相关性。的。ET增强了ADSCs在梗死心肌中的有益作用，这与更高的ADSCs保留有关。这些发现突出了ET在ADSC的心肌保留和梗塞后心脏重塑减弱中的重要性。