Galangin targets HSP90β to alleviate ulcerative colitis by controlling fatty acid synthesis and subsequent NLRP3 inflammasome activation

  • Impact factors: 6.575
  • Publication: MOLECULAR NUTRITION & FOOD RESEARCH
  • Author:Ling Yang, Xing-yu Ma, Ke-xin Mu, Yue Dai, Xia yufeng, Zhi-feng Wei
  • DOI citation-doi:10.1002/mnfr.202200755
  • Date:2023-04-01

Scope : The purpose of this research was 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, we used publicly available gene expression data and molecular biology techniques. The results showed that the expression of HSP90β was significantly increased in the mucosal biopsies of UC patients and in the colons of colitis mice, and that there was a significant correlation between HSP90β levels and disease severity. Then, Gal was found to bind directly to HSP90β and downregulate the level of p-AKT, as well as the stability and oligomerization of HSP90β, indicating Gal as an HSP90β inhibitor. Moreover, our findings revealed that HSP90β plays a critical role in controlling UC, and that Gal can alleviate colitis by inhibiting HSP90β and perturbing FAS-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. This article is protected by copyright. All rights reserved

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