The effect of red grape seed extract on the experimental model of ulcerative colitis in male albino rats: a histological, immunohistochemical and biochemical study

Background: Ulcerative colitis (UC) is a chronic inflammatory disorder of the large bowel. Red grape seed extract (GSE) has antioxidative, anti-inflammatory and antimicrobial activities. Aim of the work: This study was designed to evaluate the protective properties of GSE on an animal model of acetic acid-induced UC. Materials and methods: Rats were divided into three groups: group I – the control group; group II – the UC group in which UC was induced by a single intracolonic injection of 2 ml of 3% acetic acid; and group III – the GSE-treated group in which rats were administered GSE at 400 mg/kg/day, orally for 4 days, after induction of UC. Colon sections were subjected to H E, and immunohistochemical staining of vascular endothelial growth factor (VEGF) and α-smooth muscle actin (α-SMA). Tumour necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-10 were determined in blood by enzyme-linked immunosorbent assay. Results: The UC group showed patchy mucosal ulceration, mononuclear cell infiltration extending to the muscularis externa, increased blood vessels in the mucos a and wide separation of muscle fibers in the muscularis externa. U C significantly increased the plasma levels of proinflammatory cytokines TN F-α and IL-6 and significantly decreased immunoregulatory cytokine IL-10 level in plasma. On histologic assessment it was observed that GSE protected the colon from acetic acid-induced UC by preserving colonic crypts and their lining epithelium while decreasing mononuclear cell infiltration. This histological improvement was associated with a significant decrease in the plasma levels of TN F-α and IL-6 and a significant increase in plasma IL-10 level. Moreover, GSE significantly decreased the VEGF and α-SMA immunostaining in colonic tissues as compared with the UC group. Conclusion: This study proved the protective effect of GSE in experimentally induced UC in rats.