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毛蕊异黄酮通过调节IL-33/ST2轴预防NLRP3诱导的肠道纤维化。

Calycosin prevents NLRP3-induced gut fibrosis by regulating IL-33/ST2 axis.

作者信息

Liao Xiujun, Xie Haiting, Yu Saojun

机构信息

Department of Colorectal Surgery and Oncology, Key Laboratory of Cancer Prevention and Intervention, Ministry of Education, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.

出版信息

Heliyon. 2024 Apr 25;10(9):e30240. doi: 10.1016/j.heliyon.2024.e30240. eCollection 2024 May 15.

DOI:10.1016/j.heliyon.2024.e30240
PMID:38726105
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11078877/
Abstract

Intestinal interstitial fibrosis is a core event of inflammatory bowel disease (IBD) development. Calycosin has been recognized to carry various therapeutic bioactivities. However, the role of calycosin in intestinal interstitial fibrosis remains to be illustrated. This aim of this study was to explore the effects of calycosin on intestinal interstitial fibrosis in IBD and the underlying mechanisms. The and in vivo models were established by using TNBS-induced mouse IBD model and co-culture of intestinal epithelial cells and intestinal interstitial cells; moreover, lentivirus-mediated knockdown of NLRP3 expression was applied. The results showed that calycosin significantly improved the intestinal interstitial fibrosis of TNBS-induced IBD. Mechanistically, calycosin downregulated NLRP3 expression and inhibited the activation of IL-33/ST2 signaling in intestinal epithelial cells, which subsequently impedes intestinal interstitial cell migration and activation by regulating the secretion of IL-33/ST2 signaling-induced fibrosis mediators. Notably, combination of calycosin and NLRP3 signaling blockade improved the intestinal interstitial fibrosis extent. Altogether, this study suggests calycosin can improve intestinal interstitial fibrosis by downregulating NLRP3-IL-33/ST2 signaling, reducing inflammation and decreasing pro-fibrotic factors' secretion, which provides a new perspective for therapeutic options of IBD.

摘要

肠道间质纤维化是炎症性肠病（IBD）发展的核心事件。毛蕊异黄酮已被认为具有多种治疗生物活性。然而，毛蕊异黄酮在肠道间质纤维化中的作用仍有待阐明。本研究的目的是探讨毛蕊异黄酮对IBD肠道间质纤维化的影响及其潜在机制。通过使用TNBS诱导的小鼠IBD模型以及肠道上皮细胞和肠道间质细胞共培养建立体内和体外模型；此外，应用慢病毒介导的NLRP3表达敲低。结果表明，毛蕊异黄酮显著改善了TNBS诱导的IBD的肠道间质纤维化。机制上，毛蕊异黄酮下调NLRP3表达并抑制肠道上皮细胞中IL-33/ST2信号的激活，随后通过调节IL-33/ST2信号诱导的纤维化介质的分泌来阻碍肠道间质细胞的迁移和激活。值得注意的是，毛蕊异黄酮与NLRP3信号阻断的联合使用改善了肠道间质纤维化程度。总之，本研究表明毛蕊异黄酮可通过下调NLRP3-IL-33/ST2信号、减轻炎症和减少促纤维化因子的分泌来改善肠道间质纤维化，这为IBD的治疗选择提供了新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/56ae0c7c2328/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/136ab42ed5e8/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/8bdba4767cb4/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/bf45d3be632e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/0bf3c691ed94/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/1fe6e8e268ec/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/56ae0c7c2328/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/136ab42ed5e8/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/8bdba4767cb4/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/bf45d3be632e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/0bf3c691ed94/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/1fe6e8e268ec/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b2/11078877/56ae0c7c2328/gr6.jpg

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