Department of Cardiology, The Sixth Affiliated Hospital, School of Medicine, South China University of Technology, Foshan.
Eur J Histochem. 2024 Jun 27;68(3):4021. doi: 10.4081/ejh.2024.4021.
Cardiomyocyte apoptosis is a complex biological process involving the interaction of many factors and signaling pathways. In hypoxic environment, cardiomyocytes may trigger apoptosis due to insufficient energy supply, increased production of oxygen free radicals, and disturbance of intracellular calcium ion balance. The present research aimed to investigate the role of microRNA-29b1 (miR-29b1) in hypoxia-treated cardiomyocytes and its potential mechanism involved. We established an in vitro ischemia model using AC16 and H9C2 cardiomyocytes through hypoxia treatment (1% O2, 48 h). Cell apoptosis was evaluated by flow cytometry using Annexin V FITC-PI staining assay. Moreover, we used Western blot and immunofluorescence analysis to determine the expression of Bcl-2, Bax caspase-3 and Cx43 proteins. We found that miR-29b1 protected AC16 and H9C2 cells from hypoxia-induced injury as evidence that miR-29b1 attenuated the effects of hypoxia treatment on AC16 and H9C2 cell apoptosis after hypoxia treatment. In conclusion, our findings suggest that miR-29b1 may have potential cardiovascular protective effects during ischemia-related myocardial injury.
心肌细胞凋亡是一个涉及多种因素和信号通路相互作用的复杂生物学过程。在低氧环境中，由于能量供应不足、氧自由基生成增加以及细胞内钙离子平衡紊乱，心肌细胞可能会触发凋亡。本研究旨在探讨微小 RNA-29b1 (miR-29b1) 在缺氧处理的心肌细胞中的作用及其潜在的机制。我们通过低氧处理（1% O2，48 h）建立了 AC16 和 H9C2 心肌细胞的体外缺血模型。使用 Annexin V FITC-PI 染色法通过流式细胞术评估细胞凋亡。此外，我们还使用 Western blot 和免疫荧光分析来确定 Bcl-2、Bax caspase-3 和 Cx43 蛋白的表达。我们发现 miR-29b1 可保护 AC16 和 H9C2 细胞免受低氧诱导的损伤，这表明 miR-29b1 可减轻低氧处理对 AC16 和 H9C2 细胞凋亡的影响。总之，我们的研究结果表明，miR-29b1 在与缺血相关的心肌损伤期间可能具有潜在的心血管保护作用。
