In vivo and Computational Evaluation of Brassica oleracea Mitigation on Lead Acetate-Mediated Pancreatic Damage on Adult Male Wistar Rats: A Molecular Docking, ADMET and Drug Likeness Studies

Abstract

Lead acetate exposure induces oxidative stress and pancreatic damage, representing a critical public health concern. Brassica oleracea is recognized for its antioxidant and protective bioactivities, but its efficacy against lead-induced pancreatic toxicity requires further evaluation. This study investigates the in vivo protective effects of Brassica oleracea on pancreatic damage in adult male Wistar rats and explores the molecular docking, ADMET, and drug-likeness profiles of its key bioactive compounds against relevant pancreatic protein targets. The in vivo study demonstrates that Brassica oleracea extract has significant ameliorative effects against lead acetate-induced pancreatic toxicity in Wistar rats. The moderate dose of Brassica oleracea extract (Group D) provided the most substantial improvements in both biochemical markers and histological features, suggesting that this dosage offers an optimal balance between antioxidant activity and pancreatic recovery. Molecular docking revealed strong binding affinities ranging from -5.1 to -11.7 kcal/mol, with rutin exhibiting the highest affinity at -11.7 kcal/mol against multiple pancreatic enzymes, while neoxanthin and apigenin showed affinities up to -8.9 and -7.8 kcal/mol, respectively. ADMET analysis indicated favorable absorption and metabolism profiles for apigenin, with lower toxicity risks compared to neoxanthin and rutin. Drug-likeness evaluations favored apigenin, which complied with Lipinski’s and other key rules. These findings suggest that Brassica oleracea exerts protective effects against lead acetate-mediated pancreatic injury, with its bioactive compounds, particularly rutin and apigenin, exhibiting strong molecular interactions and promising pharmacological profiles. Further studies are warranted to develop these compounds as potential therapeutic agents.