NLRP3 炎性小体依赖性细胞焦亡被认为参与了年龄相关的异氟醚诱导认知障碍的机制。
NLRP3 inflammasome-dependent pyroptosis is proposed to be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment.
机构信息
Department of Anesthesiology, Shanghai Pudong New Area People's Hospital, Shanghai, 201200, China.
Wannan Medical College, Anhui, 241003, China.
出版信息
J Neuroinflammation. 2018 Sep 14;15(1):266. doi: 10.1186/s12974-018-1299-x.
Abstract
Wang Z et al. recently published a paper, titled "Critical role of NLRP3-caspase-1 pathway in age-dependent isoflurane-induced microglial inflammatory response and cognitive impairment". The finding in this paper is consistent with our previous study on NLRP3-caspase-1 pathway. Here, we propose that NLRP3 inflammasome-dependent pyroptosis may be involved in the mechanism of age-dependent isoflurane-induced cognitive impairment and discuss that inhibiting NLRP3 inflammasome activation with a novel inhibitor MCC950 may ameliorate age-dependent isoflurane-induced neuro-inflammation.
摘要
王志等人最近发表了一篇题为“NLRP3-caspase-1 通路在年龄依赖性异氟醚诱导的小胶质细胞炎症反应和认知障碍中的关键作用”的论文。该研究结果与我们之前关于 NLRP3-caspase-1 通路的研究一致。在这里，我们提出 NLRP3 炎性体依赖性细胞焦亡可能参与年龄依赖性异氟醚诱导的认知障碍的机制，并讨论了用新型抑制剂 MCC950 抑制 NLRP3 炎性体的激活可能改善年龄依赖性异氟醚诱导的神经炎症。
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