Brain ischaemia is one of the leading causes of mortality and disability worldwide, and the damage caused by ischaemia not only induces primary damage but also that induced by ischaemia-reperfusion (I/R) injury. Multiple processes including inflammation and oxidative stress response play important roles in the development of brain ischaemia injury. Sevoflurane is a well-known volatile anaesthetic, and a recent study discovered the role of sevoflurane in suppression of the inflammation response process via inhibition of inflammatory infiltrates and production, maintaining the balance of cytokine responses, although the possible mechanism was not fully clear. NLRC3 is a member of the nucleotide-binding domain and leucine-rich repeat containing (NLR) family, and it has been regarded as a regulator of the inflammation process via the regulation of inflammasome formation, which is an initiator of inflammatory events. In the present study, we found that overexpression of NLRC3 reduced the apoptosis in a cellular model of ischaemia reperfusion, and the expression of pro-inflammatory cytokines was also decreased. Further study found that these effects might be mediated by the TRAF6/TLR4/NF-kB signalling pathway. Thus, we speculate that overexpression might enhance the effect of sevoflurane in inhibiting the inflammatory response process in an ischaemia reperfusion model, which might be a new therapeutic strategy.

中文翻译：

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NLRC3过表达增强七氟醚对缺血再灌注细胞模型炎症的抑制作用

脑缺血是世界范围内导致死亡和残疾的主要原因之一，缺血造成的损害不仅会引起原发性损伤，还会引起缺血-再灌注（I/R）损伤。包括炎症和氧化应激反应在内的多个过程在脑缺血损伤的发展中起着重要作用。七氟醚是一种众所周知的挥发性麻醉剂，最近的一项研究发现七氟醚在抑制炎症反应过程中的作用是通过抑制炎症浸润和产生，维持细胞因子反应的平衡，尽管可能的机制尚不完全清楚。NLRC3 是核苷酸结合域和富含亮氨酸重复序列 (NLR) 家族的成员，并且它被认为是通过调节炎性体形成来调节炎症过程的，炎性体是炎症事件的始发者。在本研究中，我们发现 NLRC3 的过表达减少了缺血再灌注细胞模型中的细胞凋亡，并且促炎细胞因子的表达也降低了。进一步研究发现，这些效应可能是由 TRAF6/TLR4/NF-kB 信号通路介导的。因此，我们推测过表达可能会增强七氟醚在缺血再灌注模型中抑制炎症反应过程的作用，这可能是一种新的治疗策略。并且促炎细胞因子的表达也降低。进一步研究发现，这些效应可能是由 TRAF6/TLR4/NF-kB 信号通路介导的。因此，我们推测过表达可能会增强七氟醚在缺血再灌注模型中抑制炎症反应过程的作用，这可能是一种新的治疗策略。并且促炎细胞因子的表达也降低。进一步研究发现，这些效应可能是由 TRAF6/TLR4/NF-kB 信号通路介导的。因此，我们推测过表达可能会增强七氟醚在缺血再灌注模型中抑制炎症反应过程的作用，这可能是一种新的治疗策略。