Abstract
Ulcerative colitis (UC) is a non-specific inflammatory bowel disease characterized by ulcers and erosions in the colonic mucosa, leading to a chronic cycle with alternating periods of remission and exacerbation. Ascribed to its elusive etiology, primary therapy is limited to symptomatic treatment. Consequently, there is a pressing need to identify novel therapeutic agents for UC. Lamivudine, a nucleoside analog known for its antiviral properties and Long Interspersed Nuclear Element 1 (LINE-1) inhibitory effects, was investigated for its potential anti-inflammatory role in UC. Thus, this study aimed to investigate the anti-inflammatory effect of lamivudine on DSS (Dextran Sulphate Sodium)-induced ulcerative colitis (UC) in mice. Briefly, the mice were randomly assigned to the control group, the model group, or the lamivudine group. Following the administration of the predefined treatments, the mice were monitored, and the disease activity index (DAI) score was calculated. Moreover, histological analysis was performed to examine the efficacy of lamivudine in alleviating colitis-induced damage to the large intestine. Additionally, hematoxylin-eosin (HE) staining was performed to detect pathological alterations in intestinal tissues. Finally, the levels of IL-6, IL-17, IL-10, and TNF-α were measured using enzyme-linked immunosorbent assay (ELISA). The results revealed that the DAI score and enteritis pathological score were significantly lower in the lamivudine group compared to the model group (P < 0.05). Additionally, lamivudine significantly down-regulated the expression of the inflammatory factors IL-6, IL-17, and TNF-α in intestinal tissues and concomitantly up-regulated the expression of the anti-inflammatory factor IL-10. Lastly, lamivudine significantly attenuated the symptoms of colitis and the level of intestinal inflammation in mice and exerted anti-inflammatory effects.