首页> 美国卫生研究院文献>Biomolecules Therapeutics >Anthocyanin Extracts from Black Soybean (Glycine max L.) Protect Human Glial Cells Against Oxygen-Glucose Deprivation by Promoting Autophagy
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Anthocyanin Extracts from Black Soybean (Glycine max L.) Protect Human Glial Cells Against Oxygen-Glucose Deprivation by Promoting Autophagy

机译:黑大豆(Glycine max L.)花青素提取物通过促进自噬保护人胶质细胞免受氧葡萄糖剥夺

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摘要

Anthocyanins have received growing attention as dietary antioxidants for the prevention of oxidative damage. Astrocytes, which are specialized glial cells, exert numerous essential, complex functions in both healthy and diseased central nervous system (CNS) through a process known as reactive astrogilosis. Therefore, the maintenance of glial cell viability may be important because of its role as a key modulator of neuropathological events. The aim of this study was to investigate the effect of anthocyanin on the survival of glial cells exposed to oxidative stress. Our results demonstrated that anthocyanin extracts from black soybean increased survival of U87 glioma cells in a dose dependent manner upon oxygen-glucose deprivation (OGD), accompanied by decrease levels of reactive oxygen species (ROS). While treatment cells with anthocyanin extracts or OGD stress individually activated autophagy induction, the effect was significantly augmented by pretreatment cells with anthocyanin extracts prior to OGD. The contribution of autophagy induction to the protective effects of anthocyanin was verified by the observation that silencing the Atg5 expression, an essential regulator of autophagy induction, reversed the cytoprotective effect of anthocyanin extracts against OGD stress. Treatment of U87 cells with rapamycin, an autophagy inducer, increased cell survival upon OGD stress comparable to anthocyanin, indicating that autophagy functions as a survival mechanism against oxidative stress-induced cytotoxicity in glial cells. Our results, therefore, provide a rationale for the use of anthocyanin as a preventive agent for brain dysfunction caused by oxidative damage, such as a stroke.
机译:花青素作为饮食中的抗氧化剂,已被广泛关注,以预防氧化损伤。星形胶质细胞是特殊的神经胶质细胞,通过一种称为反应性星形胶质增生的过程,在健康和患病的中枢神经系统(CNS)中均发挥许多重要的复杂功能。因此,由于神经胶质细胞作为神经病理学事件的关键调节剂,其作用可能是重要的。这项研究的目的是研究花色苷对暴露于氧化应激的神经胶质细胞存活的影响。我们的结果表明,黑豆中的花色苷提取物以依赖于氧-葡萄糖剥夺(OGD)的剂量依赖性方式增加了U87胶质瘤细胞的存活,并伴随着活性氧(ROS)水平的降低。虽然用花青素提取物或OGD胁迫处理细胞可单独激活自噬诱导,但在OGD之前用花青素提取物预处理细胞可显着增强效果。通过观察到沉默自噬诱导的必需调节剂Atg5表达逆转了花色素提取物对OGD胁迫的细胞保护作用,证实了自噬诱导对花色苷保护作用的贡献。用雷帕霉素(一种自噬诱导剂)处理U87细胞,与花青素相比,在OGD胁迫下可提高细胞存活率,这表明自噬是一种抗氧化应激诱导的神经胶质细胞毒性的存活机制。因此,我们的结果为使用花青素作为预防由氧化性损伤(如中风)引起的脑功能障碍的预防剂提供了理论依据。

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