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首页> 外文期刊>Drug Design, Development and Therapy >Tanshinone IIA Ameliorates Progression of CAD Through Regulating Cardiac H9c2 Cells Proliferation and Apoptosis by miR-133a-3p/EGFR Axis
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Tanshinone IIA Ameliorates Progression of CAD Through Regulating Cardiac H9c2 Cells Proliferation and Apoptosis by miR-133a-3p/EGFR Axis

机译：丹参酮IIA通过调节MIR-133A-3P / EGFR轴来调节心脏H9C2细胞增殖和细胞凋亡来改善CAD的进展

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Background: Coronary artery disease (CAD) leads to the highest mortality worldwide, seriously threatening human health. Tanshinone IIA (Tan IIA), which could be extracted from Danshen, is applied in the treatment of cardiovascular and cerebrovascular diseases. MicroRNAs (miRNAs, miRs) play pivotal roles in cell proliferation and cell apoptosis of the cardiovascular system. The aim of the present study was to explore the role of Tan IIA in CAD in vitro and the underlying molecular mechanism. Methods: Real-time polymerase chain reaction (RT-PCR) and Western blot were used for the detection of miRNA/mRNA and protein, respectively. Target genes of miR-133a-3p were searched in TargetScan, and the targeting relationship was verified by dual-luciferase reporter assay. Cell proliferation was determined using a Cell Counting Kit-8 (CCK-8) and EdU labeling. Cell apoptosis was detected by flow cytometry and TUNEL staining. Results: In the present study, lower miR-133a-3p level and higher epidermal growth factor receptor (EGFR; the target of miR-133a-3p) level were found in H2O2-induced H9c2 cells. In addition, Tan IIA upregulated miR-133a-3p and downregulated EGFR expression. Moreover, Tan IIA promoted cell proliferation and suppressed apoptosis and enhanced G0/G1, which was reversed by miR-133a-3p inhibitor, while siRNA-EGFR abolished the effects induced by miR-133a-3p in H2O2-induced H9c2 cells. Conclusion: Tan IIA reversed H2O2-induced cell proliferation reduction, cell apoptosis induction, and G0/G1 arrest reduction in H9c2 cells by miR-133a-3p/EGFR axis. The findings suggested a potential molecular basis of Tan IIA in treating patients with CAD.
机译：背景：冠状动脉疾病（CAD）导致全世界的最高死亡率，严重威胁人类健康。可以从丹参提取的丹参酮IIA（Tan Iia）用于治疗心血管和脑血管疾病。 MicroRNA（MiRNA，MIRS）在细胞增殖和心血管系统细胞凋亡中发挥枢转作用。本研究的目的是探讨Tan Iia在体外CAD中的作用和潜在的分子机制。方法：实时聚合酶链反应（RT-PCR）和蛋白质印迹分别用于检测miRNA / mRNA和蛋白质。在Tar​​getScan中搜索miR-133a-3p的靶基因，并通过双荧光素酶报告酶测定验证靶向关系。使用细胞计数试剂盒-8（CCK-8）和EDU标记测定细胞增殖。通过流式细胞术和TUNEL染色检测细胞凋亡。结果：在本研究中，在H2O2诱导的H9C2细胞中发现了下miR-133a-3p水平和更高表皮生长因子受体（EGFR; miR-133a-3p）水平的水平。此外，TAN IIA上调MIR-133A-3P和下调的EGFR表达。此外，TAN IIA促进了细胞增殖和抑制的凋亡和增强的G0 / G1，其被MIR-133A-3P抑制剂反转，而siRNA-EGFR废除了MIR-133A-3P在H2O2诱导的H9C2细胞中诱导的作用。结论：MIR-133A-3P / EGFR轴线卷曲IIA逆转H2O2诱导的细胞增殖降低，细胞凋亡诱导和H9C2细胞的G0 / G1抑制。该研究结果表明Tan Iia治疗CAD患者的潜在分子基础。

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