摘要
目的探讨黄芩苷对H_(9)C_(2)心肌细胞缺氧损伤的保护作用和分子机制。方法利用CoCl_(2)对H_(9)C_(2)心肌细胞建立缺氧复氧模型。MTT实验和流式细胞术分别检测经黄芩苷处理后缺氧模型细胞活力和凋亡比例。蛋白质印迹实验检测凋亡蛋白变化情况。结果CoCl_(2)可明显降低H_(9)C_(2)细胞的细胞活力,使用1000μmol/L的CoCl_(2)处理并建立H_(9)C_(2)细胞缺氧复氧损伤模型。黄芩苷预处理可提高H_(9)C_(2)细胞活力并抑制凋亡,且呈浓度依赖性。黄芩苷保护心肌细胞作用依赖于miR-133b上调。结论黄芩苷对CoCl_(2)引起的心肌细胞缺氧复氧损伤具有保护作用,可提高细胞活力并抑制细胞凋亡;黄芩苷可提高细胞miR-133b水平进而保护心肌细胞。
Objective To investigate the protective effect of baicalin on hypoxia injury on H_(9)C_(2) cardiomyocytes.Methods The hypoxia-reoxygenation model of H_(9)C_(2) cardiomyocytes was established by CoCl_(2).The viability and apoptosis rate of hypoxic model cells which were treated with baicalin were detected by MTT assay and flow cytometry.The changes of apoptosis-related proteins were detected by Western Blotting.Results CoCl_(2) significantly reduced the cell viability of H_(9)C_(2) cardiomyocytes.The concentration of 1000μmol/L was used in subsequent experiments to establish the hypoxic-reoxygenation injury model of H_(9)C_(2) cardiomyocytes.Baicalin pretreatment increased the activity of H_(9)C_(2) cardiomyocytes and inhibited apoptosis in a concentration-dependent manner.The protective effect of baicalin on cardiomyocytes was depended on the upregulation of miR-133b.Conclusion Baicalin had a protective effect on cardiomyocytes hypoxia-reoxygenation injury induced by CoCl_(2),which could enhance cell viability and inhibit cell apoptosis.Baicalin could protect cardiomyocytes by increasing the expression of miR-133b.
作者
崔春婷
张建丽
黄颖
CUI Chunting;ZHANG Jianli;HUANG Ying(The Medical Group of Zhengzhou,First People′s Hospital,Zhengzhou 450000,Henan,China)
出处
《中西医结合心脑血管病杂志》
2021年第4期565-568,共4页
Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
