ArticleTranslational pediatrics2026
A preliminary study on NLRP3 activation and the interventional effects of MCC950 in Con A-induced EAH mice.
Article in Translational pediatrics, 2026. 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
Background: MCC950 is a selective inhibitor of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome; however, its effects have not been explored in concanavalin A (Con A)-induced experimental autoimmune hepatitis (EAH) in mice. This study aims to investigate the involvement of the NLRP3 inflammasome pathway in the pathogenesis of Con A-induced EAH and to assess the therapeutic potential and mechanistic actions of MCC950 in this model. Methods: An EAH mouse model was established via Con A injection to investigate its pathogenesis. Mice were divided into four groups: control, MCC950, Con A, and Con A + MCC950. Liver and blood samples were collected at 0, 6, 12, and 24 hours post-injection. Multiple techniques were employed, including hematoxylin and eosin (HE) staining, enzyme-linked immunosorbent assay (ELISA), western blot, quantitative real-time polymerase chain reaction (qPCR), immunohistochemistry (IHC), and a FAM-FLICA caspase-1 activity assay. These approaches were used to evaluate liver histopathology, serum transaminase levels, expression of NLRP3 inflammasome pathway components, and the extent of pyroptosis. Results: In the Con A-induced EAH mouse model, significant increases in serum transaminase levels, the extent of liver histopathological damage, the expression of NLRP3, caspase-1, interleukin (IL)-1β, and IL-18, as well as pyroptosis activity levels, were observed at 12 hours post-injection compared to baseline (0 hours) (P<0.05). Following MCC950 treatment, all these parameters were markedly reduced relative to the Con A-only group (P<0.05), indicating a protective effect of NLRP3 inhibition in this model. Conclusions: MCC950 exerts a hepatoprotective effect in the Con A-induced EAH mouse model by suppressing the NLRP3 inflammasome pathway and reducing pyroptosis.
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