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Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
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Cyanidin-3,5-O-Glucoside Alleviates DSS-Induced Colon Barrier Dysfunction and Fibrosis Through Autophagy-Associated
Zi-Xian Wang1,2, Qiu-Ping Huang1, Wei Wu3
1Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Health, Guilin Medical University, Guilin, 541199, China.
Applied Biochemistry and Biotechnology
|January 4, 2026
Summary
Cyanidin-3,5-O-glucoside (C35G) significantly improved ulcerative colitis (UC) symptoms in mice by reducing inflammation and oxidative stress. It also restored the intestinal barrier and prevented fibrosis through antioxidant and autophagy-regulating pathways.
Area of Science:
- Gastroenterology
- Molecular Biology
- Pharmacology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by intestinal inflammation, barrier dysfunction, and fibrosis.
- Current treatments for UC have limitations, necessitating the exploration of novel therapeutic agents.
- Cyanidin-3,5-O-glucoside (C35G) is a plant-derived anthocyanin with potential anti-inflammatory and antioxidant properties.
Purpose of the Study:
- To investigate the therapeutic effects of C35G on a dextran sodium sulfate (DSS)-induced mouse model of UC.
- To elucidate the underlying mechanisms of C35G action, including its impact on intestinal inflammation, mucosal barrier integrity, fibrogenesis, oxidative stress, and autophagy.
Main Methods:
- Induction of UC in mice using 2.5% DSS.
- Administration of C35G for 28 days.
- Assessment of clinical symptoms, serum inflammatory markers (IL-1β, IL-6, IL-17A, IL-18, TNF-α), and intestinal barrier function (Zo1, Claudin1, Occludin).
- Analysis of oxidative stress markers (SOD, catalase, MDA) and the Nrf2/Keap1 pathway.
- Evaluation of intestinal fibrosis markers (α-SMA, Collagen I) and NLRP3 inflammasome activation.
- Investigation of autophagy-related proteins (LC3-II, Beclin 1, p-AMPK, ULK1, p62, p-Akt, p-mTOR).
Main Results:
- C35G treatment significantly improved UC clinical symptoms and reduced disease activity.
- C35G elevated colonic mRNA levels of tight junction proteins, restoring mucosal barrier integrity.
- C35G modulated the Nrf2/Keap1 pathway, increasing antioxidant enzyme expression and reducing oxidative stress.
- C35G inhibited NLRP3 inflammasome activation, leading to reduced expression of fibrotic factors and attenuated intestinal fibrosis.
- C35G stimulated autophagy in intestinal epithelial tissues via the AMPK/Akt/mTOR/ULK1 pathway.
Conclusions:
- C35G demonstrates significant therapeutic potential for ulcerative colitis.
- C35G exerts its protective effects by reducing oxidative stress, inflammation, and fibrosis, and by restoring intestinal barrier function.
- The mechanisms involve modulation of the Nrf2/Keap1 pathway and regulation of autophagy via the AMPK/Akt/mTOR/ULK1 pathway.
