Protective effects of scutellarin in experimental colitis in rats

Ulcerative colitis (UC) is an inflammatory bowel disease of unknown etiology for which effective treatments are lacking. Scutellarin is a flavonoid with anti-apoptotic, antioxidant and anti-inflammatory effects. We investigated the possible protective effects of scutellarin on UC induced by acetic a...

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Bibliographic Details
Published in:Biotechnic & histochemistry Vol. 98; no. 6; p. 432
Main Authors: Aksit, Hasan, Aksit, Dilek, Altun, Eren
Format: Journal Article
Language:English
Published: England 18-08-2023
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Summary:Ulcerative colitis (UC) is an inflammatory bowel disease of unknown etiology for which effective treatments are lacking. Scutellarin is a flavonoid with anti-apoptotic, antioxidant and anti-inflammatory effects. We investigated the possible protective effects of scutellarin on UC induced by acetic acid in rats. We used five groups of male rats: control, scutellarin, UC, UC + scutellarin, UC + sulfasalazine. Colonic mucosal inflammation was evaluated microscopically. Malondialdehyde (MDA), superoxide dismutase (SOD) activity, total antioxidant status (TAS), nitric oxide (NO), interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and DNA fragmentation levels were measured. Colon tissue sections were evaluated using immunohistochemistry for Bcl-2 and Bax, TUNEL staining and histopathology. Pretreatment with scutellarin significantly reduced histological damage. Scutellarin significantly reduced serum and tissue levels of MDA, NO, IL-6 and TNF-α, and increased enzymatic activity of SOD and TAS. Scutellarin suppressed apoptosis by down-regulation of Bax, reduction of DNA fragmentation and increased expression of Bcl-2. Apoptosis was increased, while antioxidant enzymes were significantly decreased; some histopathologic disorders also were seen in the UC group. Administration of scutellarin ameliorated the pathological and biochemical alterations caused by UC in rats. We found that scutellarin might be protective against UC by down-regulating pro-inflammatory cytokines and suppressing apoptosis and oxidative stress.
ISSN:1473-7760
DOI:10.1080/10520295.2023.2224061