TY -的A2 Izadpanah Esmael盟——他,Xue-mei盟——周,阎真盟盛,李烁AU - Jing-jie AU -王,青盟——张、冯PY - 2020 DA - 2020/11/19 TI -鞣花酸通过抑制保护多巴胺神经元NLRP3 Inflammasome激活小胶质细胞SP - 2963540六世- 2020 AB -神经炎症病理过程中起着关键作用的帕金森病(PD)。nod样受体蛋白3 (NLRP3) inflammasome高度位于小胶质细胞,参与神经炎症的过程。的激活NLRP3 inflammasome已被证实为帕金森病的进展。因此,抑制NLRP3 inflammasome激活PD治疗可能是一个重要的切入点。鞣花酸(EA)是一种天然多酚被广泛发现在柔软的水果、坚果、和其他植物组织与抗炎,抗氧化,神经保护属性。然而,机制EA-mediated抗炎和神经保护尚未完全阐明。在这项研究中,一个脂多糖(LPS)诱导大鼠多巴胺(DA)神经损伤模型来确定执行EA保护DA神经元的影响。此外,DA神经元MN9D细胞系和小胶质细胞BV-2行了探索是否通过NLRP3-dependent EA-mediated神经保护机制。结果表明,EA改善LPS-induced DA大鼠黑质神经元损失。此外,抑制小胶质NLRP3 inflammasome信号激活参与EA-generated神经保护,就是明证以下的观察。 First, EA reduced NLRP3 inflammasome signaling activation in microglia and subsequent proinflammatory cytokines’ excretion. Second, EA-mediated antineuroinflammation and further DA neuroprotection from LPS-induced neurotoxicity were not shown upon microglial NLRP3 siRNA treatment. In conclusion, this study demonstrated that EA has a profound effect on protecting DA neurons against LPS-induced neurotoxicity via the suppression of microglial NLRP3 inflammasome activation. SN - 1942-0900 UR - https://doi.org/10.1155/2020/2963540 DO - 10.1155/2020/2963540 JF - Oxidative Medicine and Cellular Longevity PB - Hindawi KW - ER -