Neuro Protective Effects of Red Grape Seed Extract (RGSE) on Cerebral cortex and Hippocampus oxidative stress marker enzymes and histological changes against D-galactose-induced Neurotoxicity

Abstract

Objectives: To investigate the biochemical and histopathological characteristics of neurotoxicity in offspring from neurotoxin-exposed pregnant rats and to evaluate the neuroprotective potential of red grape seed extract (RGSE) against this neurotoxicity.
Aim The study aimed to assess the impact of neurotoxicity on the cerebellum and determine the possible neuroprotective role of red grape seed extract (RGSE) in mitigating oxidative stress and cellular damage in the cerebellum.
Materials and Methods: The study was conducted using 48 male pups divided into four experimental groups: Group I (Control) received saline treatment, Group II was treated with RGSE at a dose of 400 mg/kg, Group III was treated with D-Galactose (D-Gal) at 500 mg/kg, and Group IV received a combination of D-Gal (500 mg/kg) and RGSE (400 mg/kg). The cerebellar hemispheres from each group were dissected and analyzed to assess oxidative stress markers perform histological and histopathological examinations and conduct behavioral assessments.
Results: D-Gal treatment resulted in cell damage, decreased nuclear size in cerebellar tissue and markedly elevated oxidative stress markers in offspring. Nonetheless, RGSE therapy enhanced structural integrity and oxidative stress indicators, indicating RGSE's neuroprotective potential.
Discussion: Neurotoxicity in the cerebellum increases oxidative stress and cellular damage in offspring exposed to D-Gal. RGSE's antioxidant activities ameliorate oxidative stress indicators and histological structure, indicating a potential neuroprotective role.
Conclusion: Red grape seed extract demonstrated a protective effect against neurotoxicity in the cerebellum of D-Gal-exposed rats, likely due to its potent antioxidant action. These findings highlight the potential of RGSE as a therapeutic agent to mitigate neurotoxic damage, specifically targeting the cerebellum in neurotoxicity cases during prenatal development.