Protective mechanisms of 6-gingerol in dextran sulfate sodium-induced chronic ulcerative colitis in mice

被引:42
作者
Ajayi, B. O. [1 ]
Adedara, I. A. [1 ]
Farombi, E. O. [1 ]
机构
[1] Univ Ibadan, Coll Med, Drug Metab & Toxicol Res Labs, Dept Biochem, Ibadan, Nigeria
关键词
6-Gingerol; ulcerative colitis; -catenin; oxidative stress; antioxidant; INFLAMMATORY-BOWEL-DISEASE; OXIDATIVE STRESS; ANTIOXIDANT; GLUTATHIONE; HEPATOTOXICITY; EXPRESSION; PREVENTION; KOLAVIRON; CYTOKINES; CANCER;
D O I
10.1177/0960327117751235
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Ulcerative colitis (UC) is a relapsing and remitting inflammatory disease of the colon, with an increasing incidence worldwide. 6-Gingerol (6G) is a bioactive constituent of Zingiber officinale, which has been reported to possess various biological activities. This study was designed to evaluate the role of 6G in chronic UC. Chronic UC was induced in mice by three cycles of 2.5% dextran sulfate sodium (DSS) in drinking water. Each cycle consisted of 7 days of 2.5% DSS followed by 14 days of normal drinking water. 6G (100 mg/kg) and a reference anti-colitis drug sulfasalazine (SZ) (100 mg/kg) were orally administered daily to the mice throughout exposure to three cycles of 2.5% DSS. Administration of 6G and SZ significantly prevented disease activity index and aberrant crypt foci formation in DSS-treated mice. Furthermore, 6G and SZ suppresses immunoexpression of tumor necrosis factor alpha, interleukin-1, inducible nitric oxide synthase, Regulated on activation, normal T cell expressed and secreted (RANTES), and Monocyte chemoattractant protein-1 (MCP-1) in the DSS-treated mice. 6G effectively protected against colonic oxidative damage by augmenting the antioxidant status with marked decrease in lipid peroxidation levels in DSS-treated mice. Moreover, 6G significantly inhibited nuclear factor kappa B (P65), p38, cyclooxygenase-2, and -catenin whereas it enhanced IL-10 and adenomatous polyposis coli expression in DSS-treated mice. In conclusion, 6G prevented DSS-induced chronic UC via anti-inflammatory and antioxidative mechanisms and preservation of the Wnt/-catenin signaling pathway.
引用
收藏
页码:1054 / 1068
页数:15
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