Authors: Anthony Monday Agesin , Afolabi Clement Akinmoladun
DOI: https://doi.org/10.55006/biolsciences.2025.5201
Abstract
Eriodictyol offers essential protection to the brain but its effect in diabetes-induced neurologic dysfunction is poorly known. Diabetes was induced in male Wistar rats by administering 10% fructose in the drinking water for fourteen days followed by single intraperitoneal injection of 40 mg/kg body weight streptozotocin. Separate groups of diabetic rats were post-treated with varying doses of eriodictyol (0.25, 0.5 and 1.0 mg/kg) for 14 days. Thereafter, the animals were sacrificed; the hippocampi were carefully separated and processed for biochemical estimations and histopathological examination. The weight, blood glucose level, and glycated hemoglobin were determined using standard methods. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), Acetylcholinesterase (AChE) and Na+/K+-ATPase activities were evaluated. Reduced glutathione (GSH), protein carbonyl (PC) levels and the extent of lipid peroxidation (LPO) were also evaluated. Also, histopathological examination was carried out on the hippocampi brain region. Eriodictyol significantly (p<0.0001) reduced the high blood glucose level and glycated hemoglobin in the diabetic rats. There was a significant (p<0.0001) increase in SOD, CAT, GPx, Na+/K+-ATPase activities and weight as well as GSH level but, decrease in AChE activity and extent of LPO, and PC levels of diabetic rats post-treated with the flavonoid. These results were consistent with the histopathological findings which showed significant attenuation of neuronal cell death in diabetic rats post-treated with the flavonoid. The data established for the first time, the ameliorative potential of eriodictyol on oxidative imbalance and histopathological changes against fructose/stz-induced type-2 diabetic rats.
Link to Full Text: https://irrespub.com/biolsciences/index.php/1/article/view/220
