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Polysaccharides of Atractylodes Macrocephala Koidz effectively improve the EpCAM+/- genotype-related inflammatory
Cunjie Kong1, Sitong Zhou2, Changlong Xu3
1Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Guangdong Pharmaceutical University, Guangzhou, 510006, PR China; School of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center, Guangzhou, 510006, PR China.
Abstract:
The diminished EpCAM increases the susceptibility to inflammatory bowel disease (IBD). PAMK (polysaccharides of Atractylodes macrocephala Koidz) demonstrates the promotion for the intestinal health. To study the efficacy and mechanism of PAMK on mitigating IBD related to the downregulated EpCAM, it was administrated to the dextran sulfate sodium (DSS)-treated both WT and EpCAM+/- mice. DSS caused more pronounced damage to the mucosal muscular layer in the EpCAM+/- mice, increased the activity of MAPKs and upregulated the MMPs and inflammatory cytokines, but downregulated the tight junction-related proteins, STAT1, STAT6, and IRF1 in colonic tissues of the heterozygotes compared to the WT mice. After treatment with PAMK, colonic inflammation was effectively ameliorated in the DSS-induced both WT and heterozygous mice, with significant increased colon length, decreased inflammatory cells infiltration in the colonic mucosa and lamina propria, repaired colonic epithelial tight junctions, decreased activities of MAPKs and levels of MMPs, and PAMK administration promoted the reactivation of JAK-STAT-IRF1 pathway in the DSS-treated heterozygotes. Furthermore, PAMK altered the intestinal microbiota in the DSS-induced both WT and heterozygous mice, increasing the Akkermansiaceae particularly. In conclusion, PAMK could improve the colonic inflammation in not only WT mice but also EpCAM+/- mice via modulating the gut microbiota.
Insights
Polysaccharides of Atractylodes macrocephala Koidz (PAMK) can improve intestinal health and mitigate inflammatory bowel disease (IBD) by modulating gut microbiota, even in mice with reduced EpCAM expression.
Area of Science:
- Gastroenterology
- Immunology
- Microbiology
Background:
- Diminished EpCAM expression exacerbates susceptibility to inflammatory bowel disease (IBD).
- Polysaccharides of Atractylodes macrocephala Koidz (PAMK) are known to promote intestinal health.
Purpose of the Study:
- To investigate the efficacy and underlying mechanisms of PAMK in mitigating IBD, particularly in the context of downregulated EpCAM.
- To assess PAMK's effects on dextran sulfate sodium (DSS)-induced colitis in wild-type (WT) and EpCAM heterozygous (EpCAM+/-) mice.
Main Methods:
- Administration of PAMK to DSS-treated WT and EpCAM+/- mice.
- Evaluation of colonic tissue damage, inflammatory markers, MAPK activity, matrix metalloproteinases (MMPs), tight junction proteins, and JAK-STAT-IRF1 pathway.
- Analysis of changes in intestinal microbiota composition.
Main Results:
- DSS induced more severe colonic damage in EpCAM+/- mice, characterized by increased MAPK activity, MMPs, and inflammatory cytokines, alongside downregulated tight junction proteins and STAT signaling.
- PAMK treatment ameliorated colitis in both WT and EpCAM+/- mice, increasing colon length, reducing inflammation, repairing tight junctions, decreasing MAPK/MMP activity, and reactivating the JAK-STAT-IRF1 pathway in EpCAM+/- mice.
- PAMK administration modulated the gut microbiota, notably increasing Akkermansiaceae abundance in both mouse models.
Conclusions:
- PAMK effectively improves colonic inflammation in DSS-induced IBD models, irrespective of EpCAM expression levels.
- PAMK exerts its therapeutic effects by restoring gut barrier integrity, suppressing inflammatory signaling, and modulating the intestinal microbiota.
- PAMK represents a potential therapeutic agent for IBD, with benefits extending to individuals with reduced EpCAM expression.
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