Myrica salicifolia Hochst. ex A. Rich. suppress acetic acid-induced ulcerative colitis in rats by reducing TNF-alpha and interleukin-6, oxidative stress parameters and improving mucosal protection

• Published in: Human & experimental toxicology Vol. 41; p. 9603271221102518
• Main Authors: Rehman, NU, Ansari, MN, Palla, AH, Karim, A, Imam, F, Raish, M, Hamad, AM, Noman, M
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.01.2022; Sage Publications Ltd
• Subjects: Acetic acid; Acetic Acid - metabolism; Acetic Acid - toxicity; Animals; Catalase; Colitis - chemically induced; Colitis, Ulcerative - chemically induced; Colitis, Ulcerative - drug therapy; Colitis, Ulcerative - pathology; Colon - metabolism; Cytokines; Developing countries; Disease; Gastrointestinal diseases; Glutathione; Inflammatory bowel disease; Inflammatory bowel diseases; Inflammatory Bowel Diseases - metabolism; Inflammatory Bowel Diseases - pathology; Interleukin 6; Interleukin-6 - metabolism; Interleukins; LDCs; Lipid peroxidation; Lipids; Myrica; Myrica - metabolism; Natural products; Oxidative Stress; Parameters; Peroxidation; Prednisolone; Pretreatment; Rats; Side effects; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Ulcerative colitis; anti-inflammatory; ulcerative colitis; Myrica salicifolia; acetic acid colitis; tumor necrosis factor-α; interleukin-6
• ISSN: 0960-3271; 1477-0903
• DOI: 10.1177/09603271221102518

Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) with rising prevalence in developing countries, and limited success of current therapies, natural products have immense potential for therapy due to their “disease modifying and side-effect neutralizing” potential. Myrica salicifolia is traditionally used for gastrointestinal diseases and have reported antiinflammatory activities, but its use in IBD has not yet been studied. Therefore, in the present study, the effects of the root extract of M. salicifolia (Ms.Cr) were investigated using the acetic acid-induced UC model in rats. For 6 days, the rats were given either vehicle (10 mL/kg), lower (200 mg/kg), and higher (400 mg/kg) doses of Ms.Cr, or the positive control drug (prednisolone; 2 mg/kg) orally. A single dosage of 5% acetic acid (1.0 mL) was administered intrarectally to rats on day 6 to induce UC. Disease activity index (DAI), histological observations, the biochemical parameters related to oxidative stress, and specific cytokines such as interleukin-6 (IL-6) and the tumor necrosis factor-α (TNF-α) were determined to assess the effect of Ms.Cr. In comparison to the AA-induced colitis rats, Ms.Cr’s pretreatment significantly decreased DAI, colonic ulceration, and inflammatory score. Total glutathione levels and catalase activity were considerably recovered in the colitis group treated with Ms.Cr, whereas enhanced lipid peroxidation in colon tissues was significantly decreased. Moreover, Ms.Cr pretreatment also caused inhibition of the activation of IL-6 and TNF-α in the colonic tissues of respective groups. Based on these findings, Ms.Cr might be developed to treat UC in the future.