ArticleJournal of inflammation research2025
MCC950 Alleviates Experimental Autoimmune Neuritis by Inhibiting NLRP3 Inflammasome Activity and Down-Regulating Interleukin-23/Interleukin-17 Axis Expression.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Guillain-Barré syndrome (GBS), an autoimmune disease involving the peripheral nervous system, is the most common and severe acute paralytic neuropathy. However, the exact pathogenesis remains unclear. The aim of this study was to reveal the role of the NLRP3 inflammasome in regulating the Interleukin-23/Interleukin-17 axis (IL-23/IL-17 axis) in experimental autoimmune neuritis (EAN) and to explore the potential of the NLRP3 inflammasome as a drug target for the treatment of GBS. Methods: We first evaluated the expression of NLRP3 inflammasome-related genes in peripheral blood mononuclear cells (PBMCs) of GBS patients using real-time quantitative polymerase chain reaction (qPCR). Subsequently, MCC950, a NLRP3 inflammasome inhibitor, was used to detect its therapeutic effect on EAN rats induced by P2 Results: We observed that the expression of NLRP3 inflammasome related genes was increased in the peripheral blood of patients with GBS. In the EAN rat model, inhibition of NLRP3 inflammasome with MCC950 not only alleviated neurological symptoms, decreased peripheral nerve CD4 Conclusion: In the study, we demonstrated that NLRP3 inflammasome is involved in the injury of experimental autoimmune neuritis by up-regulating the expression of IL-23/IL-17 axis. This discovery provides strong evidence for the NLRP3 inflammasome as a drug target for GBS.
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