Scutellarin Protects against Myocardial Ischemia-reperfusion Injury by Enhancing Aerobic Glycolysis through miR-34c-5p/ALDOA Axis.

Pub Date : 2024-04-01 Epub Date: 2024-05-24 DOI:10.4103/ijabmr.ijabmr_415_23

Yijia Xiang, Zhongjiao Xu, Renyi Qian, Daying Wu, Li Lin, Jiayi Shen, Pengchong Zhu, Fenghui Chen, Chong Liu

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Abstract

Background: Aerobic glycolysis has recently demonstrated promising potential in mitigating the effects of ischemia-reperfusion (IR) injury. Scutellarin (Scu) possesses various cardioprotective properties that warrant investigation. To mimic IR injury in vitro, this study employed hypoxia/reoxygenation (H/R) injury.

Methods and results: First, we conducted an assessment of the protective properties of Scu against HR in H9c2 cells, encompassing inflammation damage, apoptosis injury, and oxidative stress. Then, we verified the effects of Scu on the Warburg effect in H9c2 cells during HR injury. The findings indicated that Scu augmented aerobic glycolysis by upregulating p-PKM2/PKM2 levels. Following, we built a panel of six long noncoding RNAs and seventeen microRNAs that were reported to mediate the Warburg effect. Based on the results, miR-34c-5p was selected for further experiments. Then, we observed Scu could mitigate the HR-induced elevation of miR-34c-5p. Upregulation of miR-34c-5p could weaken the beneficial impacts of Scu in cellular viability, inflammatory damage, oxidative stress, and the facilitation of the Warburg effect. Subsequently, our investigation revealed a decrease in both ALDOA mRNA and protein levels following HR injury, which could be restored by Scu administration. Downregulation of ALDOA or Mimic of miR-34c-5p could reduce these effects induced by Scu.

Conclusions: Scu provides cardioprotective effects against IR injury by upregulating the Warburg effect via miR-34c-5p/ALDOA.

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黄芩苷通过 miR-34c-5p/ALDOA 轴增强有氧糖酵解保护心肌缺血再灌注损伤

背景：有氧糖酵解最近在减轻缺血再灌注（IR）损伤的影响方面表现出了巨大的潜力。黄芩苷（Scutellarin，Scu）具有多种心脏保护特性，值得研究。为了在体外模拟红外损伤，本研究采用了缺氧/再氧合（H/R）损伤：首先，我们在 H9c2 细胞中评估了 Scu 对红外损伤的保护特性，包括炎症损伤、细胞凋亡损伤和氧化应激。然后，我们验证了 Scu 在 HR 损伤过程中对 H9c2 细胞沃伯格效应的影响。研究结果表明，Scu通过上调p-PKM2/PKM2水平来促进有氧糖酵解。随后，我们建立了一个包含 6 种长非编码 RNA 和 17 种 microRNA 的研究小组，这些 RNA 据报道可介导沃伯格效应。根据结果，我们选择了 miR-34c-5p 进行进一步实验。然后，我们观察到 Scu 可以缓解 HR 诱导的 miR-34c-5p 的升高。miR-34c-5p 的上调会削弱 Scu 对细胞活力、炎症损伤、氧化应激和沃伯格效应的促进作用。随后，我们的研究发现，HR 损伤后，ALDOA mRNA 和蛋白水平都会下降，而通过服用 Scu 可以恢复。下调ALDOA或模拟miR-34c-5p可减少Scu诱导的这些效应：结论：Scu通过miR-34c-5p/ALDOA上调沃伯格效应，对红外损伤具有心脏保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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