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Mechanism by which oleracein E alleviates TNBS-induced ulcerative colitis
Yun Huang1,2, Yu Su1, Rong Qin1
1Department of Gastroenterology, Affiliated Yan'an Hospital of Kunming Medical University.
Oleracein E (OE) effectively treats ulcerative colitis (UC) by reducing inflammation and oxidative stress. This compound improves intestinal barrier function and alleviates colitis symptoms in rat models.
Area of Science:
- Gastroenterology
- Pharmacology
- Molecular Biology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by intestinal barrier dysfunction, inflammation, and oxidative stress.
- Current treatments for UC have limitations, necessitating the exploration of novel therapeutic agents.
Purpose of the Study:
- To investigate the therapeutic potential of oleracein E (OE) in ameliorating 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced ulcerative colitis (UC).
Main Methods:
- UC models were established using lipopolysaccharide (LPS) in Caco-2 cells and TNBS in rats.
- Inflammatory markers (IL-1β, TNF-α, IL-6), oxidative stress markers (CAT, MPO, MDA), and ROS levels were assessed.
- Western blotting analyzed the Nrf2/HO-1 pathway, tight junction proteins, and apoptosis-related proteins.
- Histopathology (HE staining) and apoptosis (TUNEL staining) evaluated tissue damage and cell death.
Main Results:
- Oleracein E significantly reduced inflammatory factors (IL-1β, IL-6, TNF-α) and oxidative stress markers (MPO) while increasing antioxidant enzyme activity (CAT).
- OE treatment upregulated Nrf2/HO-1 pathway proteins, enhanced tight junction protein expression (ZO-1, Occludin, claudin-2), and inhibited apoptosis.
- Histological examination revealed that OE significantly decreased the severity of TNBS-induced colitis in rats.
Conclusions:
- Oleracein E demonstrates significant therapeutic effects against ulcerative colitis.
- OE ameliorates intestinal barrier injury, reduces inflammation and oxidative stress by activating the Nrf2/HO-1 pathway.
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