Flavonoids from Potentilla anserina protect H9C2 cells from hypoxia/reoxygenation injury by inhibiting mitochondrial apoptosis
文献类型: 外文期刊
作者: Yan, Yingying 1 ; Zhang, Yuhong 1 ; Zhang, Wenhui 1 ; Zhang, Jifeng 2 ;
作者机构: 1.Xizang Acad Agr & Anim Husb Sci XZAAAS, Inst Agriprod Dev & Food Sci IAPDFS, 157 Nongke Rd, Lhasa 850032, Tibet, Peoples R China
2.Xizang Univ, Sch Ecol & Environm, Lhasa, Peoples R China
关键词: Potentilla anserina flavonoids; hypoxia; myocardial cells; oxidative stress; mitochondrial apoptosis
期刊名称:INTERNATIONAL JOURNAL OF FOOD SCIENCE AND TECHNOLOGY ( 影响因子:3.1; 五年影响因子:3.5 )
ISSN: 0950-5423
年卷期: 2025 年 60 卷 1 期
页码:
收录情况: SCI
摘要: Potentilla anserina L., a valued traditional Chinese medicinal herb and edible plant, has a long history of use for its antioxidant and immunomodulatory properties. Flavonoids extracted from the tuberous roots of P. anserina (silverweed cinquefoil root flavonoids, SCR-F) exhibit protective effects against hypoxia/reoxygenation (H/R) injury in H9C2 cells. In our study, we observed that H/R injury reduces cell viability, increases lactate dehydrogenase release, and elevates levels of reactive oxygen species (ROS) and malondialdehyde (MDA). The protective action of SCR-F on H/R-injured H9C2 cells was concentration-dependent, with efficacy increasing alongside dosage. Notably, the strongest protective effect occurred at a concentration of 208.32 mu g/ml of SCR-F. Treatment with SCR-F significantly improved cell viability decreased ROS and MDA levels, and enhanced the activity of antioxidant enzymes, including catalase, superoxide dismutase, and glutathione peroxidase (GSH-px). Furthermore, SCR-F upregulated the expression of the anti-apoptotic protein Bcl-2, downregulated the pro-apoptotic protein Bax, and decreased caspase-3 and -9 activity. A reduction in voltage-dependent anion channel 1protein coding gene (VDAC)1 expression was also observed, suggesting inhibition of the mitochondrial apoptotic pathway. Our findings indicate that SCR-F protects H9C2 cells from H/R injury by reducing oxidative stress and mitochondrial-mediated apoptosis, underscoring its potential as a therapeutic agent for hypoxia-induced myocardial damage.
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