Kolaviron attenuates Dextran sulphate sodium-induced colitis by enhancing the expression of MUC-2.

Ulcerative colitis, a chronic inflammatory bowel disease, is a complex and multifactorial disease with unknown etiology that remains challenging in its management due to pathophysiological complexity and limited success with conventional therapies such as 5-aminosalicylic acid, corticosteroids, and anti-TNF-α antibodies. This study examines the therapeutic potential of Kolaviron, a biflavonoid complex from Garcinia kola, with a novel focus on its effect on colonic MUC-2 expression, a key component of the intestinal mucus barrier, together with its known antioxidant and anti-inflammatory actions in dextran sulphate sodium (DSS)-induced colitis in a Wistar rat model. Rats were randomly divided into 4 groups (n = 5 per group): Group 1 (Control) received vehicle (DMSO); Groups 2, 3, and 4 were administered 5% (w/v) DSS orally and received DMSO, kolaviron, or sulfasalazine (200 mg/kg), respectively. Kolaviron significantly reduced disease activity index, oxidative stress markers, myeloperoxidase activity, TNF-α, IL-6, and lipid peroxidation. It also improved colonic histoarchitecture and remarkably enhanced the expression of MUC-2. In silico docking analysis showed strong binding affinities of Kolaviron to NF-κB and phospholipase C, pointing to its contribution in the regulation of molecular pathways for MUC-2 expression. Kolaviron significantly reduced the disease activity index and colonic oxidative stress by enhancing antioxidant levels and decreasing myeloperoxidase activity, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and lipid peroxidation, with the novel enhancement of MUC-2 expression, highlighting its potential role in restoring mucosal barrier integrity.