Endocrine Abstracts

Background: Cadmium chloride (CdCl₂) is a pervasive environmental toxicant that provokes pancreatic oxidative stress, mitochondrial-dependent apoptosis and β-cell dysfunction, with downstream hyperglycemia and islet disorganization.

Methods: Twenty-five adult male Wistar rats (n = 5/group) were allocated: Group 1 (control, feed/water); Group 2 (CdCl₂, 3 mg/kg i.p., three doses on alternate days); Group 3 (Garcinia kola ethanolic extract, 100 mg/kg orally for 14 days); Group 4 (co-treatment: CdCl₂ + G. kola); Group 5 (post-treatment: CdCl₂ then G. kola). Body weights were recorded during the study. At termination fasting blood was collected for glucose measurement, animals were humanely euthanized by cervical dislocation, and pancreata were excised, weighed, and divided: portions homogenized for oxidative (e.g., MDA, SOD), inflammatory (e.g., TNF-α) and hormonal assays (insulin, glucagon, somatostatin); remaining tissue was fixed for histology and Bcl-2 immunohistochemistry.

Results & Discussion: CdCl₂ produced progressive body-weight loss, pancreatic atrophy, fasting hyperglycemia and lowered circulating insulin with histological acinar/islet degeneration; these changes corresponded with a shift toward pro-apoptotic signaling (decreased Bcl-2 / increased Bax-ratio) described for cadmium exposure. Garcinia kola treatment consistent with kolaviron and other G. kola reports showing antioxidant, anti-inflammatory and hypoglycemic actions partially or fully restored pancreatic weight, improved glycemic and hormonal profiles, reduced oxidative markers and enhanced Bcl-2 immunoreactivity, effects strongest in co- and post-treatment groups. Mechanistically, the extract’s biflavonoid-rich fraction likely attenuates ROS/JNK-mediated mitochondrial apoptosis and modulates inflammatory mediators, permitting islet recovery.

Conclusion: Ethanolic Garcinia kola extract mitigates CdCl₂-induced pancreatic injury via antioxidant, anti-inflammatory and anti-apoptotic pathways.