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Drug Res (Stuttg) 2017; 67(01): 20-24
DOI: 10.1055/s-0042-114572
Original Article
© Georg Thieme Verlag KG Stuttgart · New York

Carpolobia lutea G. Don (Polygalaceae) Inhibits Inflammation and Oxidative Stress in an Acetic Acid Induced Model of Rat Colitis

O. O. Abiodun
1   Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria
,
A. O. Oshinloye
1   Department of Pharmacology and Therapeutics, College of Medicine, University of Ibadan, Ibadan, Nigeria
› Author Affiliations
Further Information

Publication History

received 06 April 2016

accepted 02 August 2016

Publication Date:
14 September 2016 (online)

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Abstract

Carpolobia lutea G. Don (CL) is used in folk medicine for the treatment of inflammatory disorders. Effort in this study is to evaluate the beneficial effect of the aqueous-methanol extract of leaf of CL in a rat model of acetic acid induced colitis. Male Wistar rats were distributed into 6 groups of 7 rats each; non colitic, untreated colitic and colitic rats treated with graded doses of CL (100–800 mg/kg). Rats were pre-treated for 2 days before colitis induction and thereafter for 7 days post colitic induction. 24 h after the last treatment, animals were sacrificed and colonic inflammation was evaluated both macroscopically and biochemically. Macroscopic damage score, weight/length ratio, myeloperoxidase (MPO) activity and tumor necrotic factor alpha (TNF-α) levels, were significantly higher in untreated colitic rats in comparison with non colitic rats (P<0.05). Treatment with CL significantly reduced the macroscopic damage scores, neutrophil infiltration (MPO activity) and TNF-α level (P<0.05). In addition, C. lutea significantly prevented depletion of colonic GSH and (SOD) levels (P<0.05). It appears that the beneficial effect of methanol extract of C. lutea leaf observed in this study is dose dependent and is related to its antioxidant and anti-inflammatory activity.

Key words

Carpolobia lutea - colitis - rats - glutathione - superoxide dismutase - myeloperoxidase - tumour necrotic factor alpha (TNF-α)
 

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