Potential therapeutic effects of escin in mitigating inflammation and oxidative stress in experimentally induced ulcerative colitis in mice by acetic acid

Abstract Background Ulcerative colitis (UC) is a long-term immune-triggered disorder marked by persistent inflammation, oxidative stress, and lesions in the colonic mucosal layer. Escin, a triterpenoid saponin derived from the horse chestnut ( Aesculus hippocastanum ) tree, has been experimentally demonstrated to exhibit anti-inflammatory and antioxidant activities. Therefore, the current work aimed to assess the potential effects of escin in managing UC induced by intrarectal (I.R.) of acetic acid (AA) in mice in comparison with the customary drug sulfasalazine (SSZ). Materials and methods Escin (20 or 40 mg/kg body weight “b.w”) or SSZ (500 mg/kg b.w) was administered I.R. one hour (h), 6 h, and 12 h following the enema administration of 6% AA solution to provoke UC. Eventually, colon tissues were harvested at the final stage of the study for morphological and histological analysis, in addition to the assessment of biochemical markers. Results The UC-mice treated with escin exhibited a significant decline in macroscopic and microscopic lesions of colon tissues, colon weight-to-length ratio, mortality rate, and colonic degranulated mast cells. Additionally, escin reduced substantially malondialdehyde and nitric oxide, whereas it elevated the content of reduced glutathione and the activities of superoxide dismutase and catalase in colon tissues of UC-mice. Moreover, escin successfully declined the nuclear factor kappa B and cyclooxygenase-2 concentrations in colon tissues, and suppressed the colonic expression of interleukin (IL)-23 and IL-17 A. Conclusion Escin may offer a novel therapeutic strategy for treating UC conditions via suppressing the inflammatory process and inhibiting oxidative stress, as shown here in the experimental UC-mice.