Argon mitigates post-stroke neuroinflammation by regulating M1/M2 polarization and inhibiting NF-κB/NLRP3 inflammasome signaling

Author:

Xue Ke1,Qi Mian1,She Tongping1,Jiang Zhenglin1,Zhang Yunfeng2,Wang Xueting1,Wang Guohua1,Xu Lihua1,Peng Bin1,Liu Jiayi13,Song Xinjian3,Yuan Yuan1,Li Xia1

Affiliation:

1. Institute of Special Environmental Medicine, Co-innovation Center of Neuroregeneration, Nantong University , Nantong 226001 , China

2. Stroke Center & Department of Neurology, Affiliated Hospital of Nantong University , Nantong 226001 , China

3. Department of Rehabilitation Medicine, Affiliated Nantong Rehabilitation Hospital of Nantong University , Nantong 226002 , China

Abstract

Abstract Neuroinflammation plays a vital role in cerebral ischemic stroke (IS). In the acute phase of IS, microglia are activated towards the pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes. Argon, an inert gas, can reduce neuroinflammation and alleviate ischemia/reperfusion (I/R) injury. However, whether argon regulates M1/M2 polarization to protect against I/R injury as well as the underlying mechanism has not been reported. In this study, we analyzed the activation and polarization of microglia after I/R injury with or without argon administration and explored the effects of argon on NLRP3 inflammasome-mediated inflammation in microglia in vitro and in vivo. The results showed that argon application inhibited the activation of M1 microglia/macrophage in the ischemic penumbra and the expression of proteins related to NLRP3 inflammasome and pyroptosis in microglia. Argon administration also inhibited the expression and processing of IL-1β, a primary pro-inflammatory cytokine. Thus, argon alleviates I/R injury by inhibiting pro-inflammatory reactions via suppressing microglial polarization towards M1 phenotype and inhibiting the NF-κB/NLRP3 inflammasome signaling pathway. More importantly, we showed that argon worked better than the specific NLRP3 inflammasome inhibitor MCC950 in suppressing neuroinflammation and protecting against cerebral I/R injury, suggesting the therapeutic potential of argon in neuroinflammation-related neurodegeneration diseases as a potent gas inhibitor of the NLRP3 inflammasome signaling pathway.

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Genetics,Molecular Biology,General Medicine

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