article · Zenodo (CERN European Organization for Nuclear Research)
The pancreas is a glandular organ endowed with two main functions; an exocrine function that assists digestion and an endocrine function that modulates blood glucose concentration. Pancreatic Beta-cells produce insulin to regulate/lower blood glucose concentration, driving them into cells to be utilized. Distortions of the architecture of pancreatic Beta-cells lead to function loss; thus, preservation/restoration of their cytoarchitecture would sustain their functions. Vernonia amygdalina is a vital plant acknowledged widely for its antioxidant and anti-diabetic effects; however, its impact on the pancreas has received little attention. This study is premeditated to examine the effects of the methanolic leaf extracts of Vernonia amygdalina (MLEVA) on the cytoarchitecture of the pancreas in Alloxan-induced pancreatic toxicity. Thirty (30) adult male Wistar rats were grouped into 6 (A-F) (n=5). Group A, the control group, received feed and water only. 69 Group B received a single intraperitoneal injection of 150mg/kg of Alloxan. Groups C, D, and E received single intra-peritoneal injections of 150mg/kg of Alloxan and were then treated with 200, 300, and 400 mg/kg/day of the MLEVA, respectively. Group F received a single intraperitoneal injection of 150mg/kg of Alloxan and was orally treated with 100mg/kg/day of Vitamin E. The experiment lasted 16 days before sacrificing the animals via a median incision on the abdominal cavity, under ketamine (100mg/ml), as anesthesia, 24 hours after their last treatment. The pancreas was carefully and rapidly processed for routine H & E staining. This study recorded a 28% mortality rate after Alloxan administration, leading to degenerative histo-pathological changes in the pancreas' endocrine and exocrine compartments. 300mg/kg of MLEVA demonstrated a marked regenerative effect on the pancreas. The MLEVA is a promising agent for managing Diabetes, evidenced by its protective and therapeutic effect on Alloxan-induced pancreatic toxicity.
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DOI: 10.5281/zenodo.8046230
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