| 王文光,李 猛,王晓敏,宋秀荣,王义华,马 双,金 慧.MiR-145在低氧诱导的心肌细胞中的表达及其作用研究[J].现代生物医学进展英文版,2020,(9):1642-1647. |
| MiR-145在低氧诱导的心肌细胞中的表达及其作用研究 |
| Expression and Effect of miR-145 in the Apoptotic Neonatal Rat Cardiomyo-cytes Induced by Hypoxia |
| Received:November 03, 2019 Revised:November 25, 2019 |
| DOI：10.13241/j.cnki.pmb.2020.09.008 |
| 中文关键词: miRNA-145 心肌细胞 缺氧 凋亡 |
| 英文关键词: miRNA-145 Cardiomyocytes Hypoxia Apoptosis |
| 基金项目:国家自然科学基金项目(81860447) |
| Author Name | Affiliation | | WANG Wen-guang | Department of Cardiology, Baotou Central Hospital, Baotou, Inner Mongolia, 014040, China | | LI Meng | Department of Cardiology, Baotou Central Hospital, Baotou, Inner Mongolia, 014040, China | | WANG Xiao-min | Translational Medicine Center, Baotou Central Hospital, Baotou, Inner Mongolia, 014040, China | | SONG Xiu-rong | Department of Cardiology, Baotou Central Hospital, Baotou, Inner Mongolia, 014040, China | | WANG Yi-hua | Department of Cardiology, Baotou Central Hospital, Baotou, Inner Mongolia, 014040, China | | MA Shuang | Department of Cardiology, Baotou Central Hospital, Baotou, Inner Mongolia, 014040, China | | JIN Hui | Department of Cardiology, Baotou Central Hospital, Baotou, Inner Mongolia, 014040, China |
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| 中文摘要: |
| 摘要 目的：探讨MiR-145在低氧诱导的心肌细胞凋亡模型中的表达及其意义。方法：在正常和低氧条件下，采用RT-qPCR检测乳大鼠原代心肌细胞miR-145的表达，进一步采用miR-145抑制剂和拟似物处理心肌细胞，将细胞置于37 ℃密闭的缺氧盒中(95% N2和5% CO2)培养，采用Caspase-3活性分析和TUNEL检测心肌细胞凋亡情况。通过结扎SD大鼠冠状动脉左前降支(LAD)建立心肌缺血再灌注(I/R)模型，了解miR-145在缺血再灌注损伤中的作用。结果：miR-145过表达可抑制缺氧诱导的心肌细胞凋亡。转染miR-145抑制剂后，细胞对缺氧更敏感。缺血0.5h、1h和3h的心肌组织中miR-145的表达明显低于周围非缺血心肌组织。缺氧3h、6h、12h时 miR-145 水平明显下调。在缺血再灌注损伤模型中，mimic 组 MiR-145表达明显高于对照组，而凋亡细胞(%)和梗死面积危险区(%)明显低于对照组。结论：MiR-145可以抑制缺氧诱导的心肌细胞凋亡，减小缺血再灌注损伤导致的心肌梗死面积。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the expression and clinical significance of microRNA-145 (miR-145) in the apoptosis model of cardiomyocytes induced by hypoxia. Methods: Under normal and hypoxic conditions, the expression of miR-145 in neonatal rat cardiomyocytes was detected by RT-qPCR. miR-145 inhibitor and mimic were transfected into the primary neonatal rat cardiomyocytes. The transfected cardiomyocytes were cultured in closed anoxic box (95% N2 and 5% CO2 ) at 37 ℃. Ischemiareperfusion (I/R) of animal model was established by left anterior descending coronary artery (LAD). Results: Overexpression of miR-145 can inhibit hypoxia-induced cardiomyocyte apoptosis. The cells were more sensitive to hypoxia after transfection with miR-145 inhibitor. The levels of miR-145 in ischemic myocardium tissue were significantly lower than the surrounding non-ischemic myocardium tissue at 0.5 h, 1 h and 3 h after ischemia. The levels of miR-145 were significantly down-regulated at 3 h, 6 h, and 12 h of hypoxia. MiR-145 in mimic group was significantly higher than that of the control group, while apoptotic cells (%) and infarct size/area at risk (%) were significantly lower than that of the control group. Conclusion: Mir-145 can inhibit hypoxia-induced myocardial cell apoptosis and reduce the myocardial infarction area caused by ischemia reperfusion injury. |
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