Inhibitory Effect of Ginkgo biloba Extract on Oxidative Stress and Apoptosis of Myocardial Cells in Sepsis by Regulating miR-370/FOXO1

IF 0.9 4区 材料科学 Science of Advanced Materials Pub Date : 2024-04-01 DOI:10.1166/sam.2024.4644
Hai Lin, Yunwei Rao, Jinrong Yi
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Abstract

This research was aimed to investigate the effects of Ginkgo biloba leaf extract on oxidative stress and apoptosis in septic cardiomyocytes, focusing on the role of the miR-370/FOXO1 regulatory pathway. The major components of Ginkgo biloba leaf extract were determined using high-performance liquid chromatography. In vitro cardiomyocytes were utilized as the research subjects, with control (Con) group cardiomyocytes obtained from normal individuals, experimental (Exp) group cardiomyocytes obtained from patients with septic cardiomyocyte injury, and treatment (Tre) group cardiomyocytes obtained from septic cardiomyocyte injury patients treated with Ginkgo biloba leaf extract. Western blot and real-time fluorescence quantification techniques were employed to investigate cell apoptosis, changes in antioxidative enzymes superoxide dismutase (SOD) and malondialdehyde (MDA) levels, as well as alterations in key proteins involved in oxidative stress and the miR-370/FOXO1 regulatory pathway. The results showed that the main components of Ginkgo biloba leaf extract included total flavonoids and total Ginkgo biloba acid. Treatment with Ginkgo biloba leaf extract markedly reduced oxidative stress levels and exhibited a notable decrease in apoptosis rate. The SOD concentration in Exp group cells was greatly decreased (P <0.05), and the SOD concentration in Tre group cells was drastically inferior to that in Exp group (P <0.05). The MDA concentration in Exp group cells was notably increased (P <0.05), while the MDA concentration in Tre group cells was drastically inferior to that in Exp group (P <0.05). The levels of Caspase-3, Caspase-6, Bax/BCL-2, and FOXO1 proteins were markedly elevated in Exp group cardiomyocytes (P <0.05), while miR-370 was greatly reduced (P <0.05). In Tre group cardiomyocytes, the levels of Caspase-3, Caspase-6, Bax/BCL-2, and FOXO1 proteins were drastically inferior to those in Exp group (P <0.05), and miR-370 was notably superior to Exp group (P < 0.05). In summary, Ginkgo biloba leaf extract can inhibit oxidative stress and apoptosis in septic cardiomyocytes by modulating the miR-370/FOXO1 pathway, providing a novel approach for the treatment of septic cardiomyocyte injury.
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银杏叶提取物通过调节 miR-370/FOXO1 抑制败血症患者心肌细胞的氧化应激和凋亡
本研究旨在探讨银杏叶提取物对脓毒症心肌细胞氧化应激和凋亡的影响,重点关注miR-370/FOXO1调控途径的作用。采用高效液相色谱法测定了银杏叶提取物的主要成分。以体外心肌细胞为研究对象,对照(Con)组心肌细胞取自正常人,实验(Exp)组心肌细胞取自脓毒症心肌细胞损伤患者,治疗(Tre)组心肌细胞取自接受银杏叶提取物治疗的脓毒症心肌细胞损伤患者。采用 Western 印迹和实时荧光定量技术研究了细胞凋亡、抗氧化酶超氧化物歧化酶(SOD)和丙二醛(MDA)水平的变化,以及参与氧化应激和 miR-370/FOXO1 调控通路的关键蛋白的变化。结果表明,银杏叶提取物的主要成分包括总黄酮和总银杏酸。银杏叶提取物能明显降低氧化应激水平,显著降低细胞凋亡率。Exp 组细胞的 SOD 浓度大大降低(P <0.05),Tre 组细胞的 SOD 浓度大大低于 Exp 组(P <0.05)。Exp组细胞的MDA浓度显著升高(P<0.05),而Tre组细胞的MDA浓度则大大低于Exp组(P<0.05)。Exp组心肌细胞的Caspase-3、Caspase-6、Bax/BCL-2和FOXO1蛋白水平明显升高(P<0.05),而miR-370则大大降低(P<0.05)。在 Tre 组心肌细胞中,Caspase-3、Caspase-6、Bax/BCL-2 和 FOXO1 蛋白水平显著低于 Exp 组(P <0.05),而 miR-370 则明显高于 Exp 组(P <0.05)。综上所述,银杏叶提取物可通过调节miR-370/FOXO1通路抑制脓毒症心肌细胞的氧化应激和凋亡,为治疗脓毒症心肌细胞损伤提供了一种新方法。
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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来源期刊
Science of Advanced Materials
Science of Advanced Materials NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
自引率
11.10%
发文量
98
审稿时长
4.4 months
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