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苦参碱通过激活 AMPK/Sirt3 信号通路减轻心肌细胞缺血再灌注损伤。

Matrine attenuates cardiomyocyte ischemia-reperfusion injury through activating AMPK/Sirt3 signaling pathway.

机构信息

Department of General Medicine, Tungwah Hospital of Sun yat-sen University, Dongguan, China.

Arrhythmia Center, Ningbo First Hospital, Zhejiang, China.

出版信息

J Recept Signal Transduct Res. 2021 Oct;41(5):488-493. doi: 10.1080/10799893.2020.1828914. Epub 2020 Oct 6.

DOI:10.1080/10799893.2020.1828914
PMID:33019890
Abstract

Matrine has been found to affect cell viability and function. In the present study, we explored the cardioprotective role of matrine in cardiomyocyte damage under hypoxia/reoxygenation. , cardiomyocyte hypoxia/reoxygenation was used to mimic ischemia/reperfusion injury in the presence of matrine. After exposure to hypoxia/reoxygenation, cardiomyocyte viability was reduced and cell apoptosis was increased; this alteration was inhibited by matrine. At the molecular levels, Sirt3 and AMPK were significantly downregulated by hypoxia/reoxygenation injury whereas matrine administration was able to upregulate Sirt3 and AMPK expression and activity in the presence of hypoxia/reoxygenation. Interestingly, inhibition of Sirt3/AMPK pathway abolished the cardioprotective action of matrine on cardiomyocyte in the presence of hypoxia/reoxygenation injury, resulting into cardiomyocyte viability reduction and cell death augmentation. Altogether, our results demonstrated a novel role played by matrine in regulating cardiomyocyte viability and death in the presence of hypoxia/reoxygenation, with a potential application in the clinical practice for the treatment of patients with myocardial infarction.

摘要

苦参碱已被发现会影响细胞活力和功能。在本研究中,我们探讨了苦参碱在缺氧/复氧条件下对心肌细胞损伤的心脏保护作用。在苦参碱存在的情况下,使用心肌细胞缺氧/复氧来模拟缺血/再灌注损伤。缺氧/复氧后,心肌细胞活力降低,细胞凋亡增加;苦参碱抑制了这种改变。在分子水平上,缺氧/复氧损伤显著下调 Sirt3 和 AMPK,而苦参碱给药能够上调缺氧/复氧条件下 Sirt3 和 AMPK 的表达和活性。有趣的是,Sirt3/AMPK 通路的抑制消除了苦参碱在缺氧/复氧损伤条件下对心肌细胞的心脏保护作用,导致心肌细胞活力降低和细胞死亡增加。总之,我们的研究结果表明,苦参碱在调节缺氧/复氧条件下心肌细胞活力和死亡方面发挥了新的作用,在治疗心肌梗死患者的临床实践中具有潜在的应用价值。

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