Polysaccharides from armillariella tabescens mycelia alleviates 5-fluorouracil-induced chemotherapy-induced intestinal mucositis via inhibiting the TLR4/MyD88/NF-κB signaling pathway
10.19405/j.cnki.issn1000-1492.2025.07.016
- Author:
Mengru Yuan
1
;
Zhongxuan Gui
1
;
Xinru Wan
1
;
Wenna Zhang
2
;
Yan Chen
2
;
Mei Zhang
3
Author Information
1. Dept of Oncology Integrated Traditional Chinese and Western Medicine，The First Affiliated Hospital of Anhui Medical University，Hefei 230022
2. School of Life Sciences，Anhui University，Hefei 230601
3. Dept of Oncology Integrated Traditional Chinese and Western Medicine，The First Affiliated Hospital of Anhui Medical University，Hefei 230022; Graduate School of Anhui University of Traditional Chinese Medicine，Hefei 230012
- Publication Type:Journal Article
- Keywords:
armillariella tabescens mycelia polysaccharides;
TLR4/MyD88/NF-κB signaling pathway;
chemotherapy-induced intestinal mucositis;
5-fluorouracil;
tight junction protein;
intestinal barrier function
- From:
Acta Universitatis Medicinalis Anhui
2025;60(7):1275-1281, 1290
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate whether armillariella tabescens polysaccharides (ATPS) alleviates inflamma- tory responses and tissue damage in 5-fluorouracil ( 5-FU ) -induced chemotherapy-induced intestinal mucositis ( CIM) by inhibiting the TLR4 /MyD88 /NF-κB signaling pathway．
Methods:Thirty 8-weeks-old male C57BL/6J mice were randomly divided into five groups ( n = 6 per group) : control group，model group ，and ATPS-treated groups (low，medium，high dose : 100，200，400 mg / kg) ．Body weight changes were recorded ; Disease activity in- dex (DAI) scores were evaluated ; small intestinal length and histopathology were measured ; HE staining and his- topathological scoring were performed ; immunohistochemistry was used to detect the expression of tight junction pro- teins (ZO-1，Occludin) in the small intestine ; serum levels of inflammatory cytokines interleukin-6 ( IL-6 ) and tumor necrosis factor-alpha (TNF-α) were analyzed by enzyme-linked immunosorbent assay (ELISA) kit ; Western blot was employed to quantify ZO-1，Occludin，and TLR4 /MyD88 /NF-κB pathway-related protein TLR4，MyD88，NF-κB p65，IκBα , p-NF-κB p65，p-IκBα protein expression．
Results :Compared with the control group，mice in the model group exhibited significant reductions in body weight ，elevated DAI scores ，shortened small intestinal length，increased histopathological scores，marked downregulation of ZO-1 and Occludin expression，and elevated levels of inflammatory cytokines TNF-α and IL-6．Additionally，protein expression levels of TLR4，MyD88，p-NF- κB p65，and p-IκBα were significantly upregulated ( all P ＜0. 01 ) ． In contrast ，mice in ATPS-treated groups showed dose-dependent improvements，attenuated weight loss，reduced DAI scores，restored intestinal length，de- creased histopathological scores，upregulated ZO-1 and Occludin expression，reduced TNF-α and IL-6 levels，and downregulated TLR4，MyD88，p-NF-κB p65，and p-IκBα protein expression (all P＜0. 01) ．
Conclusion : ATPS alleviates 5-FU-induced CIM by inhibiting the TLR4 /MyD88 /NF-κB signaling pathway．
- Full text:2026030516105404961亮菌多糖通过抑制TLR4_MyD88_NF-κB信号通路缓解5-氟尿嘧啶诱导的化疗性肠黏膜炎_袁梦如.pdf
