| Abstract |
Introduction: Ulcerative colitis (UC) is subcategorized in inflammatory bowel disease (IBD). However, the etiology of UC remains unclear and current UC treatments are moderately successful with excessive side effects. Garcinia mangostana Linn. (GM) has been traditionally used for several maladies. α-Mangostin, a major active constituent in GM, has been claimed for anti-inflammatory activity. Besides, it possesses the appropriate pharmacokinetics to well distribute to colon. Objective: This study aimed to investigate anti-inflammatory potential of α-mangostin in dextran sulfate sodium (DSS)-induced UC in ICR mice. Materials and Methods: Six-week-old male ICR mice were divided into 3 groups (n=9). Some mice were intragastrically administered α-mangostin (30 mg/kg/day; MGS) for 7 consecutive days while the control (CT) and non-treatment (NT) groups were given vehicle (0.5% carboxymethylcellulose). On day 4 to 7, the MGS and NT groups were induced UC by oral administration of DSS (40 kDa) solution (6 g/kg/day). At 24 hours after the last treatments, the mouse colons were collected to examine histomorphology by hematoxylin and eosin staining and evaluate mRNA expression of tumor necrosis factor-α (Tnf-α), monocyte chemoattractant protein-1 (Mcp-1), and intercellular adhesion molecule-1 (Icam-1) by RT/real-time PCR. Results: Histological changes, including goblet cells depletion, epithelial erosion, and crypt of Lieberkühn damage, were observed in the NT group. In addition, infiltration of inflammatory cells was observed in the colonic mucosa. Notably, α-mangostin protected normal colonic structure and reduced inflammatory cells in the colon mucosa with a significant attenuation of the expressions of pro-inflammatory cytokine Tnf-α, chemokine Mcp-1, and adhesion molecule Icam-1. Discussion and Conclusion: α-Mangostin is an ultimate biochemical candidate in GM demonstrating anti-inflammatory effects; therefore, it is worth for further development as an anti-inflammatory regimen for UC treatment. |
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