【摘要】 目的探讨来源于骨髓源性心肌干细胞的外切体(MCSCs-exosomes)对成年大鼠心肌细胞体外缺氧损伤诱导凋亡的干预作用。方法将体外培养的成年大鼠心肌细胞随机分为对照组、缺氧组和MCSCs-exosomes预处理组。随后进行形态学观察、细胞计数,蛋白质印迹法检测凋亡相关蛋白(Bcl-2,bax)的表达变化,流式细胞仪检测凋亡率的变化。结果与对照组相比,缺氧组细胞凋亡相关指标均明显升高,细胞计数下降(P<0.01),Bcl-2/bax表达下调(P<0.01),凋亡细胞比例明显增多。而MCSCsexosomes预处理组可明显改善缺血缺氧损伤时的细胞活力,上调Bcl-2/bax的表达,降低凋亡细胞的比例(P均<0.05)。结论 MCSCs-exosomes预处理可以明显改善体外培养缺氧损伤诱导的成年大鼠心肌细胞的凋亡情况,其机制可能是通过抗凋亡途径减轻缺氧时细胞的损伤。更多还原

【Abstract】 Objective To observe the apoptosis of injured adult rats myocardial cells induced by ischemia and hypoxia in vitro and the biological functions of the exosomes from marrow-derived cardiac stem cells(MCSCs- exosomes). Methods Cultured adult rats myocardial cells were divided into the control group,the ischemia- hypoxia group and the MCSCs- exosomes pretreated group. In vitro,we counted the cells and detected the expression of Bcl- 2,bax by Western Blotting. The cell cycles and apoptosis were measured by flow cytometry. Results Compared with the control group,the model group showed lower cell counts(P<0.01) and higher apoptosis ratio. We also observed that the expression of Bcl- 2 / bax was decreased(P<0.01) and the cell cycle was blocked at S phase.Compared with the ischemia-hypoxia group,MCSCs-exosomes pretreated groups showed apparent tolerance to ischemic and hypoxic injury in vitro,which manifested a higher cell viability,lower apoptosis ratio,increased expression of Bcl- 2/bax and relief of the block of S phase( all P<0.05). Conclusions Ischemia and hypoxia could cause the apoptosis of cells in vitro.MCSCs- exosomes exhibited anti- apoptosis ability in vitro. All these may provide experimental evidences for the mechanisms of MCSCs-exosomes in therapy of tissue injury.更多还原