Pharmacological Activity of 6-Gingerol in Dextran Sulphate Sodium-induced Ulcerative Colitis in BALB/c Mice

被引:78
作者
Ajayi, Babajide O. [1 ]
Adedara, Isaac A. [1 ]
Farombi, Ebenezer O. [1 ]
机构
[1] Univ Ibadan, Coll Med, Dept Biochem, Drug Metab & Toxicol Res Labs, Ibadan, Nigeria
关键词
6-gingerol; colitis; inflammatory cytokines; oxidative stress; mouse; INFLAMMATORY-BOWEL-DISEASE; GLUTATHIONE; QUANTIFICATION; KOLAVIRON; GINGER; DAMAGE; RATS;
D O I
10.1002/ptr.5286
中图分类号
R914 [药物化学];
学科分类号
100705 [微生物与生化药学];
摘要
Gingerols are phenolic compounds in ginger (Zingiber officinale), which have been reported to exhibit antiinflammatory, antioxidant, and anticancer properties. The present study aimed at evaluating the possible pharmacologic activity of 6-gingerol in a mouse model of dextran sulphate sodium (DSS)-induced ulcerative colitis. Adult male mice were exposed to DSS in drinking water alone or co-treated with 6-gingerol orally at 50, 100, and 200mg/kg for 7days. Disease activity index, inflammatory mediators, oxidative stress indices, and histopathological examination of the colons were evaluated to monitor treatment-related effects of 6-gingerol in DSS-treated mice. Administration of 6-gingerol significantly reversed the DSS-mediated reduction in body weight, diarrhea, rectal bleeding, and colon shrinkage to near normal. Moreover, 6-gingerol significantly suppressed the circulating concentrations of interleukin-1 and tumor necrosis factor alpha and restored the colonic nitric oxide concentration and myeloperoxidase activity to normal in DSS-treated mice. 6-Gingerol efficiently prevented colonic oxidative damage by increasing the activities of antioxidant enzymes and glutathione content, decreasing the hydrogen peroxide and malondialdehyde levels, and ameliorated the colonic atrophy in DSS-treated mice. 6-Gingerol suppressed the induction of ulcerative colitis in mice via antioxidant and antiinflammatory activities, and may thus represent a potential anticolitis drug candidate. Copyright (c) 2015 John Wiley & Sons, Ltd.
引用
收藏
页码:566 / 572
页数:7
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