Mitigation of sodium arsenite toxicity during gastric ulcer healing by kolaviron and vitamin E: Insights from molecular docking analyses of NADPH oxidase

Sodium arsenite toxicity has been a major problem due to its extensive presence in contaminated water and food, leading to oxidative stress and formation of ulcers in the gastrointestinal tracts. This study elucidated the therapeutic actions of Kolaviron and vitamin E against toxicity of sodium arsenite during gastric ulceration, and insights into molecular docking against NADH oxidases. Experimental animals (male, n = 12, ±200) were grouped in to seven groups; I(control),II(gastric ulcer induced by acetic acid(ACIU), III(ACIU+ 5 mg/kg Sodium Arsenite(SA), IV(ACIU +SA+100 mg/kg vitamin E(ACIU+ SA+ 100 mg/kg Kolaviron(KV), VI(ACIU +KV),VII(ACIU+ Vit. E). The KV was gotten from Garcinia kola. Ulcer induced by60 % acetic acid.Kolaviron and vitamin E were administered for two weeks post-ulcer induction. The ulcer area was determined by using planimetry, while Biochemical indices, H/ATPase and NO concentration were evaluated. H and E, immunohistochemistry was done on the gastric tissue to evaluate the expression of CD31, ki67, and P53 to investigate angiogenesis, proliferation and apoptosis. Data were subjected to analysis of variance, P < 0.05. The molecular docking of Kolaviron and vitamin E against NADPH oxidases was evaluated. Finding shows that kolaviron and vitamin E significantly mitigated sodium arsenite-induced oxidative stress, and gastric ulceration, P < 0.05. In the ulcerated control animals, the ulcer areas were 0.74 ± 0.01 cm², 0.57 ± 0.08 cm², 0.53 ± 0.12 cm² and 0.24 ± 0.04 cm² while SA exposure significantly increased ulcer areas for 100.0 %, 66.7 %, 40 %, 66.7 % by days 3, 7, 14 and 21, respectively. By day 21 post-ulcer induction, Kolaviron and vitamin E had reduced ulcer areas relative to SA-treated group by 100 % respectively. Kolaviron and vitamin E significantly decrease the lipid peroxidation and increase the anti-oxidants, P < 0.05. There was enhanced angiogenesis(CD38),proliferation(Ki67),and inhibition of apoptosis(P53). Molecular docking analyses revealed that kolaviron exhibited a high binding affinity for NADPH oxidase, implicated in gastric ulcer pathogenesis. These findings suggest that kolaviron and vitamin E may be a promising agents for preventing and treating gastric ulcers induced by sodium arsenite toxicity.