1. Academic Validation
  2. Plantamajoside alleviates DSS-induced ulcerative colitis by modulating gut microbiota, upregulating CBS, and inhibiting NF-κB

Plantamajoside alleviates DSS-induced ulcerative colitis by modulating gut microbiota, upregulating CBS, and inhibiting NF-κB

  • Phytomedicine. 2025 Jul 25:143:156827. doi: 10.1016/j.phymed.2025.156827.
Yongheng Jia 1 Xianjun Liu 2 Xinyi Gao 1 Siyuan Yin 1 Kun Wu 1 Xianglong Meng 3 Hui Ren 4 Jiawei Liu 1 Zijing Liu 1 Hao Li 5 Yang Jiang 6
Affiliations

Affiliations

  • 1 Department of Gastrointestinal Colorectal and Anal Surgery, the China-Japan Union Hospital of Jilin University, No. 126 Xian Tai Street, Changchun 130000, China.
  • 2 College of Biological and Food Engineering, Jilin Engineering Normal University, No. 3050 Kaixuan Street, Changchun 130000, China; Postdoctoral Research Workstation, Changchun Gangheng Electronics Company Limited, Changchun 130000, China.
  • 3 Department of Gastroenterology, the China-Japan Union Hospital of Jilin University, No. 126 Xian Tai Street, Changchun 130000, China.
  • 4 Department of General surgery, the China-Japan Union Hospital of Jilin University, Changchun 130000, China.
  • 5 College of Biological and Food Engineering, Jilin Engineering Normal University, No. 3050 Kaixuan Street, Changchun 130000, China.
  • 6 Department of Gastrointestinal Colorectal and Anal Surgery, the China-Japan Union Hospital of Jilin University, No. 126 Xian Tai Street, Changchun 130000, China. Electronic address: jiangyang@jlu.edu.cn.
Abstract

Background: Plantamajoside (PMS) is a natural bioactive compound derived from medicinal, food homologous Plants of the genus Plantago.

Purpose and methods: This study aimed to investigate the protective effects of PMS on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice and explore the associated mechanisms.

Results: We found that PMS treatment significantly alleviated UC symptoms in mice by preventing body weight loss, increasing colon length, and reducing disease activity index scores. Moreover, PMS alleviated colonic lesions, increased the number of goblet cells, upregulated the expression of intestinal barrier proteins (ZO-1, occludin, and claudin-3), and decreased the levels of pro-inflammatory factors. PMS treatment modulated the gut microbiota by increasing the relative abundance of Bacteroidota and Verrucomicrobiota and decreasing that of Firmicutes and Proteobacteria at the phylum level. At the genus level, PMS suppressed the abundance of pathogenic bacteria, such as Turicibacter and upregulated the abundance of [Eubacterium]_xylanophilum_group. Fecal microbiota transplantation experiments further confirmed that PMS treatment alleviated UC by modulating the gut microbiota. Transcriptomic analysis of colon tissues, coupled with reverse transcription-quantitative polymerase chain reaction and western blotting, showed that PMS treatment upregulated cystathionine beta-synthase (CBS) expression and inhibited NF-κB pathway activation. In a lipopolysaccharide-induced inflammation model in RAW264.7 cells, PMS treatment inhibited the secretion of pro-inflammatory cytokines, upregulated CBS expression, and prevented NF-κB pathway activation.

Conclusion: PMS protects against UC in mice via multiple mechanisms, including modulating the gut microbiota, increasing the expression levels of CBS, and inhibiting the NF-κB pathway.

Keywords

CBS; Gut microbiota; NF-κB signaling pathway; Plantamajoside; Ulcerative colitis.

Figures
Products