title: Myrrhattenuates oxidative and inflammatory processes in acetic acid-induced ulcerative colitis.
abstract: The pathogenesis of ulcerative colitis (UC) has been associated with a weakened antioxidant capacity and increased inflammatory processes.Myrrhis traditionally used for the treatment of inflammatory diseases due to its antioxidant and anti-inflammatory properties. The present study aimed to evaluate the effects ofmyrrhon an experimental rat model of UC. UC was induced in rats using acetic acid (AA) after pre-treatment withmyrrh(125, 250 or 500 mg/kg/day) or mesalazine (MES; 300 mg/kg/day) for 7 days. The levels of various inflammatory cytokines, prostaglandin E2(PGE2) and nitric oxide (NO) in the rat colon tissues were assessed. In addition, the colonic levels of thiobarbituric acid reactive substances (TBARS) and non-protein sulfhydryl groups (NP-SH), as well as the activities of superoxide dismutase (SOD) and catalase (CAT), were estimated. Furthermore, total protein (TP) contents and the levels of DNA and RNA were measured, and histopathological changes in colonic tissues were analyzed. The results indicated that the levels of pro-inflammatory cytokines, PGE2, NO and TBARS were markedly increased. By contrast, the levels of interleukin-10, NP-SH, TP and nucleic acids, and the enzymatic activities of SOD and CAT were significantly decreased in the AA model group. In addition, pretreatment withmyrrhand MES was able to attenuate the impaired oxidative stress response and upregulation of inflammatory biomarkers. Furthermore, the enzymatic activities of SOD and CAT were near to normal in themyrrhand MES pretreated groups. The ability ofmyrrhto protect against UC was further confirmed by histopathological analysis, and the high dose ofmyrrhexerted an effect comparable to MES. In conclusion, the results of the present study suggested thatmyrrhhas potent therapeutic value in the amelioration of experimental colitis in laboratory animals by downregulating the expression of proinflammatory mediators and improving endogenous antioxidative activities.
authors.affiliation: Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
authors.forename: Amal Jamil
authors.initials: AJ
authors.lastname: Fatani
authors.affiliation: Department of Internal Medicine, Medical School, Al Maareefa Colleges, Riyadh 11461, Saudi Arabia.
authors.forename: Fatima Salih
authors.initials: FS
authors.lastname: Alrojayee
authors.affiliation: Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
authors.forename: Mihir Yogeshkumar
authors.initials: MY
authors.lastname: Parmar
authors.affiliation: Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia; Department of Biomedical Dental Sciences, College of Dentistry, University of Dammam, Dammam 31441, Saudi Arabia.
authors.forename: Hatem Mustafa
authors.initials: HM
authors.lastname: Abuohashish
authors.affiliation: Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
authors.forename: Mohammed Mahboobuddin
authors.initials: MM
authors.lastname: Ahmed
authors.affiliation: Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
authors.forename: Salim Salih
authors.initials: SS
authors.lastname: Al-Rejaie
keywords: Commiphora molmol; acetic acid; inflammatory bowel diseases; oxidative stress; ulcerative colitis