Galangin Targets HSP90β to Alleviate Ulcerative Colitis by Controlling Fatty Acid Synthesis and Subsequent NLRP3 Inflammasome Activation

Scope The purpose of this research is to investigate the specific role of HSP90 paralogs in ulcerative colitis (UC), and to explore the mechanisms behind the inhibitory effects of galangin (Gal) on UC by inhibiting HSP90β in vivo. Methods and results In order to achieve this, publicly available gene expression data and molecular biology techniques are used. The results show that the expression of HSP90β is significantly increased in the mucosal biopsies of UC patients and in the colons of colitis mice, and that there is a significant correlation between HSP90β levels and disease severity. Then, Gal is found to bind directly to HSP90β and downregulates the level of p-AKT, as well as the stability and oligomerization of HSP90β, indicating Gal as an HSP90β inhibitor. Moreover, the findings reveal that HSP90β plays a critical role in controlling UC, and that Gal can alleviate colitis by inhibiting HSP90β and perturbing fatty acid synthesis-mediated NLRP3 inflammasome activation. Conclusion These results not only provide insight into the potential therapeutic use of Gal in the treatment of UC, but also offer new perspectives on the role of HSP90β in this disease.

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