<br>中药参元丹 (SYD) 通过上调 miR-24/Bim 通路改善缺氧诱导的新生大鼠心肌细胞凋亡,Evidence-based Complementary and Alternative Medicine

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中药参元丹 (SYD) 通过上调 miR-24/Bim 通路改善缺氧诱导的新生大鼠心肌细胞凋亡
Evidence-based Complementary and Alternative Medicine Pub Date : 2022-02-03 , DOI: 10.1155/2022/5804187
Fuyong Chu ₁ , Xue Yan ₂ , Xingjiang Xiong ₃ , Mingxue Zhou ₄ , Yupei Tan ₁ , Yixuan Li ₅ , Wei Liu ₁ , Hongxu Liu ₁

Affiliation

背景：急性心肌梗死（AMI）是恶性心律失常、心力衰竭和猝死的主要原因。然而，迄今为止尚无安全有效的治疗AMI的药物。本研究旨在探讨中药神元丹（SYD）在缺氧诱导的新生大鼠心肌细胞凋亡中的作用。此外，该研究还探讨了SYD减少心肌缺血凋亡、调节miR-24/Bim通路表达的可能机制。方法：采用缺氧诱导的新生大鼠心肌细胞进行实验。这些心肌细胞用 miR-24 模拟物和 miR-24 抑制剂转染，然后与含有 SYD 的血清共培养。采用MTT和乳酸脱氢酶（LDH）测定、AnnexinV/PI双染色、流式细胞术和TUNEL染色来测定缺氧条件下的细胞活力和凋亡。此外，通过蛋白质印迹和实时定量聚合酶链反应测定缺氧诱导的心肌细胞中Bim的表达水平。结果：缺氧48小时后，心肌细胞中LDH和肌酸磷酸激酶（CPK）活性增加，细胞活力下降，miR-24表达上调。 SYD减轻了缺氧引起的心肌细胞损伤，降低了LDH和CPK活性，增加了细胞活力，并减少了新生大鼠心肌细胞的凋亡。此外，SYD 可以上调 miR-24 表达并下调 Bim 表达。 miR-24表达上调显着增强SYD的作用，从而改善心肌细胞凋亡。双荧光素酶报告基因测定和蛋白质印迹分析证实 Bim 是 miR-24 的直接靶标。结论：SYD 治疗通过上调 miR-24 表达来减少缺氧诱导的心肌细胞凋亡。这项研究为SYD促进心肌功能恢复和延缓心力衰竭发生的治疗潜力的分子机制提供了新的见解。

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Traditional Chinese Medicine Shen-Yuan-Dan (SYD) Improves Hypoxia-Induced Cardiomyocyte Apoptosis in Neonatal Rats by Upregulating miR-24/Bim Pathway

Background: Acute myocardial infarction (AMI) is the leading cause of malignant arrhythmia, heart failure, and sudden death. However, safe and effective drugs for the treatment of AMI are unavailable to date. The present study aimed to investigate the role of traditional Chinese medicine shen-yuan-dan (SYD) in hypoxia-induced cardiomyocyte apoptosis in neonatal rats. In addition, the study explored the possible mechanism through which SYD could reduce myocardial ischemia apoptosis and regulate the expression of the miR-24/Bim pathway. Methods: Hypoxia-induced neonatal rat cardiomyocytes were used for the experiments. These cardiomyocytes were transfected with an miR-24 mimic and an miR-24 inhibitor and then cocultured with SYD-containing serum. MTT and lactate dehydrogenase (LDH) assays, AnnexinV/PI double staining, flow cytometry, and TUNEL staining were used to determine the cell viability and apoptosis under hypoxic conditions. Furthermore, the expression level of Bim in the hypoxia-induced cardiomyocytes was determined through western blotting and quantitative real-time polymerase chain reaction. Results: After 48 h of hypoxia, LDH and creatine phosphokinase (CPK) activities increased, cell viability decreased, and miR-24 expression upregulated in the cardiomyocytes. SYD alleviated hypoxia-induced cardiomyocyte injury, decreased LDH and CPK activities, increased cell viability, and reduced apoptosis in the neonatal rat cardiomyocytes. Moreover, SYD could upregulate miR-24 expression and downregulate Bim expression. Upregulation of miR-24 expression significantly enhanced the effect of SYD, thereby improving myocardial cell apoptosis. Dual-luciferase reporter assay and western blot analysis confirmed that Bim was a direct target of miR-24. Conclusion: SYD treatment reduces hypoxia-induced myocardial apoptosis by upregulating miR-24 expression. This study provides new insights into the molecular mechanism underlying the therapeutic potential of SYD in promoting the recovery of myocardial function and delaying the incidence of heart failure.

更新日期：2022-02-03

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