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首页> 外文期刊>Journal of biochemical and molecular toxicology >Amyloid β induces NLRP3 inflammasome activation in retinal pigment epithelial cells via NADPH oxidase‐ and mitochondria‐dependent ROS production
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Amyloid β induces NLRP3 inflammasome activation in retinal pigment epithelial cells via NADPH oxidase‐ and mitochondria‐dependent ROS production

机译：淀粉样蛋白β通过NADPH氧化酶和线粒体依赖性ROS生产在视网膜色素上皮细胞中诱导NLRP3炎症活化

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摘要

Abstract Amyloid β (Aβ)‐induced chronic inflammation is believed to be a key pathogenic process in early‐stage age‐related macular degeneration (AMD). Nucleotide oligomerization domain (NOD)‐like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation triggered by Aβ is responsible for retinal pigment epithelium (RPE) dysfunction in the onset of AMD; however, the detailed molecular mechanism remains unclear. In this study, we investigated the involvement of NADPH oxidase‐ and mitochondria‐derived reactive oxygen species (ROS) in the process of Aβ 1–40 ‐induced NLRP3 inflammasome activation in LPS‐primed ARPE‐19 cells. The results showed that Aβ 1–40 could induce excessive ROS generation, MAPK/NF‐κB signaling activation and subsequently NLRP3 inflammasome activation in LPS‐primed ARPE‐19 cells. Furthermore, the inductive effect of Aβ 1–40 on NLRP3 inflammasome activation was mediated in a manner dependent on NADPH oxidase‐ and mitochondria‐derived ROS. Our findings may provide a novel insight into the molecular mechanism by which Aβ contributes to the early‐stage AMD.
机译：摘要淀粉样蛋白β（Aβ）诱导的慢性炎症被认为是早期年龄相关性黄斑变性（AMD）的关键致病方法。核苷酸寡聚化结构域（NOOD） - 样受体家族，含有3（NLRP3）炎症的吡啶结构域由Aβ触发的炎症激活是AMD发作中的视网膜颜料上皮（RPE）功能障碍。但是，详细的分子机制仍然不清楚。在这项研究中，我们研究了NADPH氧化酶和线粒体和线粒体衍生的反应性氧物质（ROS）在β1-40诱导的NLRP3炎性组活化中的过程中的参与LPS-Primed ARPE-19细胞中的方法。结果表明，Aβ1-40可以诱导过量的ROS生成，MAPK / NF-κB信号传导激活，随后在LPS引发的ARPE-19细胞中的NLRP3炎症活化。此外，以依赖于NADPH氧化酶和线粒体衍生的ROS的方式介导Aβ1-40对NLRP3炎症组活化的诱导效果。我们的研究结果可以提供对Aβ对早期AMD有助于早期AMD的分子机制的新颖洞察力。

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