Beneficial Effect of Shikonin on Experimental Colitis Induced by Dextran Sulfate Sodium in Balb/C Mice

• Published in: Evidence-based complementary and alternative medicine Vol. 2012; no. 2012; pp. 1 - 15
• Main Authors: Miguel Cerdá, José, Giner, Rosa María, Ríos, José Luis, Andújar, Isabel, Recio, María del Carmen
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01-01-2012; Hindawi Limited
• Subjects: Activation; Cancer therapies; Chemical compounds; Colon; Cyclooxygenase-2; Cytokines; Dextran; Dextran sulfate; Gastroenterology; Immune system; Inflammation; Inflammatory bowel disease; Inflammatory bowel diseases; Interleukin 6; Intestine; Lithospermum erythrorhizon; Macrophages; Mice; NF-κB protein; Oral administration; Peroxidase; Polyphenols; Prostaglandin endoperoxide synthase; Rodents; Shikonin; Sodium; Sodium sulfate; Stat3 protein; Stools; Sulfates; Transcription factors; Tumor necrosis factor; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Ulcerative colitis
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2012/271606

The naphthoquinone shikonin, a major component of the root of Lithospermum erythrorhizon, now is studied as an anti-inflammatory agent in the treatment of ulcerative colitis (UC). Acute UC was induced in Balb/C mice by oral administration of 5% dextran sodium sulfate (DSS). The disease activity index was evaluated, and a histologic study was carried out. Orally administered shikonin reduces induced UC in a dose-dependent manner, preventing the shortening of the colorectum and decreasing weight loss by 5% while improving the appearance of feces and preventing bloody stools. The disease activity index score was much lower in shikonin-treated mice than in the colitic group, as well as the myeloperoxidase activity. The expression of cyclooxygenase-2 was reduced by 75%, activation of NF-κB was reduced by 44%, and that of pSTAT-3 by 47%, as well as TNF-α, IL-1β, and IL-6 production. Similar results were obtained in primary macrophages culture. This is the first report of shikonin’s ability to attenuate acute UC induced by DSS. Shikonin acts by blocking the activation of two major targets: NF-κB and STAT-3, and thus constitutes a promising potential therapeutic agent for the management of the inflammatory bowel disease.