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首页> 外文期刊>Frontiers in Medicine >Sulforaphane Alleviates Particulate Matter-Induced Oxidative Stress in Human Retinal Pigment Epithelial Cells
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Sulforaphane Alleviates Particulate Matter-Induced Oxidative Stress in Human Retinal Pigment Epithelial Cells

机译:索林素减轻了人类视网膜色素上皮细胞中的颗粒状物质诱导的氧化胁迫

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摘要

Age-related macular degeneration (AMD) is a leading cause of blindness in the elderly, and oxidative damage to retinal pigment epithelial (RPE) cells plays a major role in the pathogenesis of AMD. Exposure to high levels of atmospheric particulate matter (PM) with an aerodynamic diameter of 2.5 μm (PM 2.5 ) causes respiratory injury, primarily due to oxidative stress. Recently, a large community-based cohort study in the UK reported a positive correlation between PM 2.5 exposure and AMD. Sulforaphane (SFN), a natural isothiocyanate found in cruciferous vegetables, has known antioxidant effects. However, the protective effects of SNF in the eye, especially in the context of AMD, have not been evaluated. In the present study, we evaluated the effect of SFN against PM 2.5 -induced toxicity in human RPE cells (ARPE-19) and elucidated the molecular mechanism of action. Exposure to PM 2.5 decreased cell viability in ARPE-19 cells in a time- and dose-dependent manner, potentially due to elevated intracellular reactive oxygen species (ROS). SFN treatment increased ARPE-19 cell viability and decreased PM 2.5 -induced oxidative stress in a dose-dependent manner. PM 2.5 -induced downregulation of serum- and glucocorticoid-inducible kinase 1 (SGK1), a cell survival factor, was recovered by SFN. PM 2.5 treatment decreased the enzymatic activities of the antioxidant enzymes including superoxide dismutase and catalase, which were restored by SFN treatment. Taken together, these findings suggest that SFN effectively alleviates PM 2.5 -induced oxidative damage in human ARPE-19 cells via its antioxidant effects, and that SFN can potentially be used as a therapeutic agent for AMD, particularly in cases related to PM 2.5 exposure.
机译:年龄相关的黄斑变性(AMD)是老年人失明的主要原因,视网膜色素上皮(RPE)细胞对氧化性损伤在AMD发病机制中起主要作用。暴露于高水平的大气颗粒物质(PM),其空气动力学直径为<2.5μm(2.5μm)引起呼吸损伤,主要是由于氧化应激。最近,英国的大型社区队列研究报告了下午2.5曝光与AMD之间的正相关。亚氟氯丙烷(SFN),在十字花植物中发现的天然异硫氰酸酯,具有已知的抗氧化作用。然而,SNF在眼睛中的保护作用,特别是在AMD的背景下尚未得到评估。在本研究中,我们评估了SFN对人RPE细胞(ARPE-19)中PM 2.5诱导的毒性的影响,并阐明了作用的分子机制。暴露于PM 2.5以时间和剂量依赖性方式在ARPE-19细胞中降低细胞活力,可能是由于细胞内反应性氧(ROS)升高。 SFN治疗增加了ARPE-19细胞活力并以剂量依赖性方式降低了PM 2.5〜5〜5诱导的氧化胁迫。 PM 2.5诱导血清和糖皮质激素诱导激酶1(SGK1)的下调,通过SFN回收细胞存活因子。 PM 2.5治疗降低了通过SFN处理恢复的超氧化物歧化酶和过氧化氢酶的抗氧化酶的酶活性。总之,这些发现表明,SFN通过其抗氧化作用有效地减轻了人ARPE-19细胞中的氧化损伤,并且SFN可能被用作AMD的治疗剂,特别是在与PM 2.5暴露有关的情况下。

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