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首页> 外文期刊>Cellular Physiology and Biochemistry >Edaravone Attenuates the Proinflammatory Response in Amyloid-?2-Treated Microglia by Inhibiting NLRP3 Inflammasome-Mediated IL-1?2 Secretion
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Edaravone Attenuates the Proinflammatory Response in Amyloid-?2-Treated Microglia by Inhibiting NLRP3 Inflammasome-Mediated IL-1?2 Secretion

机译：依达拉奉抑制NLRP3炎性体介导的IL-1？2分泌，减轻淀粉样β2处理的小胶质细胞的促炎反应。

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>Background/Aims: Microglial activation is an important pathological feature in the brains of patients with Alzheimera€?s disease (AD), and amyloid-?2 (A?2) peptides play a crucial role in microglial activation. In addition, edaravone (EDA) was recently shown to suppress oxidative stress and proinflammatory cytokine production in APPswePS1dE9 (APP/PS1) mice. However, the mechanism by which EDA inhibits the A?2-induced proinflammatory response in microglia is poorly understood. Methods: The mitochondrial membrane potential (a????m) was evaluated using JC-1 staining. Intracellular reactive oxygen species (ROS) and mitochondrial ROS levels were detected using CM-H2DCFDA and MitoSOXTM Red, respectively. The levels of CD11b, NLRP3, pro-caspase-1 and manganese superoxide dismutase (SOD-2) were observed by western blotting, and the levels of interleukin-1beta (IL-1?2) in culture supernatants were quantified using an ELISA kit. Results: A?2 induced microglia activation and mitochondrial dysfunction. In addition, mitochondrial dysfunction was associated with ROS accumulation and activation of the NLRP3 inflammasome. Importantly, A?2 induced activation of the NLRP3 inflammasome, leading to caspase-1 activation and IL-1?2 release in microglia. Moreover, EDA obviously attenuated the depolarization of a????m, reduced mitochondria-derived ROS production and increased SOD-2 activity, resulting in the suppression of NLRP3 inflammasome-mediated IL-1?2 secretion in A?2-treated microglia. Conclusion: EDA is a mitochondria-targeted antioxidant and exhibits anti-inflammatory effects on A?2-treated microglia.
机译：> 背景/目的： 小胶质细胞激活是阿尔茨海默氏病（AD）和2型淀粉样蛋白（A）的患者大脑中的重要病理特征。 2）肽在小胶质细胞活化中起关键作用。此外，最近显示依达拉奉（EDA）可抑制APPswePS1dE9（APP / PS1）小鼠的氧化应激和促炎性细胞因子的产生。但是，EDA抑制小胶质细胞中Aβ2诱导的促炎反应的机理尚不清楚。 方法： 使用JC-1染色评估线粒体膜电位（a ???? m）。分别使用CM-H2DCFDA和MitoSOX TM Red检测细胞内活性氧（ROS）和线粒体ROS水平。通过Western印迹观察CD11b，NLRP3，前胱天蛋白酶-1和锰超氧化物歧化酶（SOD-2）的水平，并使用ELISA试剂盒定量培养上清液中白细胞介素1β（IL-1？2）的水平。 结果： A？2引起小胶质细胞活化和线粒体功能障碍。此外，线粒体功能障碍与ROS的积累和NLRP3炎性小体的激活有关。重要的是，Aβ2诱导NLRP3炎性小体的激活，导致小胶质细胞中caspase-1激活和IL-1α2释放。此外，EDA明显减弱了αβm的去极化，减少了线粒体来源的ROS产生并增加了SOD-2活性，从而抑制了由Aβ2处理的小胶质细胞中NLRP3炎性体介导的IL-1α2分泌的抑制。 。 结论： EDA是针对线粒体的抗氧化剂，对经Aβ2处理的小胶质细胞具有抗炎作用。

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