ArticleFrontiers in pharmacology2025
Gut microbiota and HMGB1/NLRP3/GSDMD inflammasome-dependent pyroptosis: mechanisms by physcion ameliorates alcoholic liver fibrosis.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Lipopolysaccharide and HMGB1: key regulatory factors in the pathophysiology of sepsis a mechanistic and therapeutic review.Frontiers in immunology · 2026Review
- Emodin and physcion alleviate cholestatic liver injury by targeting FXR: hepatoprotective components identified in processedFrontiers in pharmacology · 2025Article
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Authors and funding
7 authors.
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Abstract
Alcoholic liver fibrosis (ALF) developed from long-term excessive alcohol consumption, which causes inflammatory reactions, lipid accumulation and cirrhosis. An imbalance in gut microbiota is a crucial driving factor for liver fibrosis through the gut-liver axis. This study aimed to explore the effect of physcion on ALF associated with HMGB1/NLRP3 pathways and gut microbiota. C57BL/6 mice were used to establish animal model of ALF, LX-2 cells were used to establish alcohol-activated cell model, the intestinal contents of the mice were collected and analyzed by 16S rRNA sequencing. Physcion effectively ameliorated ALF-induced inflammation, collagen deposition, lipid accumulation by SirT1, AMPK phosphorylation and SREBP1 expression. Moreover, pyroptosis-related proteins (Caspase-1, IL-1β, GSDMD) were significantly reduced after physcion treatment. Interestingly, the diversity of intestinal bacteria and the abundance in physcion treatment mice was significantly higher, while the abundance of harmful bacteria was significantly lower than that in ALF mice. Importantly, it was found that physcion inhibit HMGB1/NLRP3 pathways both
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