未经证实:神经炎症在脑出血(ICH)后起重要作用。NLRP3炎性体介导的焦亡有助于神经炎症的机制。据报道,树突状细胞相关的C型凝集素-1(Dectin-1)激活会引发神经系统疾病中的炎症。然而,Dectin-1对ICH后NLRP3炎性体介导的焦亡的作用尚不清楚.这里,我们旨在探讨Dectin-1对ICH后NLRP3炎性体介导的焦亡和神经炎症的影响。
UNASSIGNED:成年雄性C57BL/6小鼠用于建立ICH模型。Laminarin,Dectin-1抑制剂用于干预.通过蛋白质印迹和免疫荧光评估Dectin-1的表达。测试脑含水量和神经行为功能以评估脑水肿和神经表现。进行蛋白质印迹以评估GSDMD-N的水平。ELISA试剂盒用于测量IL-1β和IL-18的水平。qRT-PCR和Westernblot检测NLRP3炎性体的表达,IL-1β,IL-18
未经证实:Dectin-1的表达在ICH后增加,Dectin-1在小胶质细胞上表达。此外,海带多糖对Dectin-1的抑制作用可减少脑出血后的脑水肿和神经功能缺损。此外,Dectin-1的抑制降低了焦亡相关蛋白的表达,GSDMD-N,和炎性细胞因子(IL-1β和IL-18)。机械上,Dectin-1阻断抑制NLRP3炎性体激活,从而通过在体内和体外减弱NLRP3炎性体介导的焦亡来减轻神经炎性损伤。
UNASSIGNED:我们的研究表明,Dectin-1的抑制通过减弱NLRP3炎性体介导的细胞凋亡来减轻神经炎症。
UNASSIGNED: Neuroinflammation plays an important role following intracerebral hemorrhage (ICH). NLRP3 inflammasome-mediated pyroptosis contributes to the mechanism of neuroinflammation. It has been reported that dendritic cell-associated C-type lectin-1 (Dectin-1) activation triggers inflammation in neurological diseases. However, the role of Dectin-1 on NLRP3 inflammasome-mediated pyroptosis after ICH remains unclear. Here, we aimed to explore the effect of Dectin-1 on NLRP3 inflammasome-mediated pyroptosis and neuroinflammation after ICH.
UNASSIGNED: Adult male C57BL/6 mice were used to establish the ICH model. Laminarin, an inhibitor of Dectin-1, was administered for intervention. Expression of Dectin-1 was evaluated by Western blot and immunofluorescence. Brain water content and neurobehavioral function were tested to assess brain edema and neurological performance. Western blot was conducted to evaluate the level of GSDMD-N. ELISA kits were used to measure the levels of IL-1β and IL-18. qRT-PCR and Western blot were performed to evaluate the expressions of NLRP3 inflammasome, IL-1β, and IL-18.
UNASSIGNED: The expression of Dectin-1 increased following ICH, and Dectin-1 was expressed on microglia. In addition, inhibition of Dectin-1 by laminarin decreased brain edema and neurological impairment after ICH. Moreover, inhibition of Dectin-1 decreased the expression of pyroptosis-related protein, GSDMD-N, and inflammatory cytokines (IL-1β and IL-18). Mechanistically, Dectin-1 blockade inhibits NLRP3 inflammasome activation, thereby alleviating neuroinflammatory injury by attenuating NLRP3 inflammasome-mediated pyroptosis both in vivo and in vitro.
UNASSIGNED: Our
study indicates that the inhibition of Dectin-1 alleviates neuroinflammation by attenuating NLRP3 inflammasome-mediated pyroptosis after ICH.