【摘要】 目的 探讨富集mi R-29b的外泌体在心肌梗死（MI）后抑制心室重构的影响。方法 通过体外转染技术制备富集mi R-29b的外泌体，并通过尾静脉注射将其递送至心肌梗死的小鼠。实验分为四组：正常对照组、MI模型组、外泌体治疗组和富集mi R-29b的外泌体治疗组。采用超声心动图、组织病理学染色及免疫印迹法等手段评估心功能、心室重构程度及相关分子的变化。结果 与MI模型组相比，富集mi R-29b的外泌体治疗组显著改善了心肌梗死后的心功能，具体表现为左心室射血分数和左心室缩短分数显著提高。同时，心肌纤维化及胶原沉积显著减少。mi R-29b在心肌组织中的表达显著上调，胶原蛋白I和胶原蛋白III的表达显著下调。结论 小鼠尾静脉注射富集mi R-29b的外泌体，通过调控心肌纤维化，显著抑制心肌梗死后的心室重构。本研究为利用富集特定mi RNA的外泌体治疗心血管疾病提供了新的视角和潜在的治疗策略。更多还原

【Abstract】 Objective To investigate the role and underlying mechanisms of exosomes(EXOs) enriched with miR-29b in inhibiting post-myocardial infarction(MI) ventricular remodeling. Methods miR-29b-enriched EXOs were engineered via in vitro transfection and administered to MI-induced mice through tail vein injection. The experiment was divided into four groups: normal control, MI model, EXO-treated, and miR-29b-enriched EXO-treated. Cardiac function, ventricular remodeling,and related molecular mechanisms were assessed using echocardiography, histopathological staining, and Western blot analysis.Results Compared to the MI model group, miR-29b-enriched EXO treatment significant improved post-MI cardiac function,in the miR-29b-enriched EXO group. miR-29b overexpression in cardiac tissue correlated with downregulated collagen I and collagen III expression. Conclusion Tail vein injection of miR-29b-enriched EXOs effectively suppresses ventricular remodeling post-MI by targeting myocardial fibrosis. This study highlights the potential of miRNA-engineered exosomes as a novel therapeutic strategy for cardiovascular diseases.更多还原