Esculin's Antioxidant Effect on Lead Acetate-Induced Neurotoxicity in the C57BL/6 Mice's Hippocampus and Cortex

Abstract

Lead exposure to heavy metals is linked to significant neuronal damage due to reactive oxygen species-mediated
oxidative stress. This research examined esculin's possible neuroprotective effects on the C57bl/6 model of lead
(Pb)-induced brain damage. The experiment included four groups of mice: control, lead acetate-treated (10 mg/kg),
lead acetate plus esculin (10 mg/kg + 15 mg/kg), and esculin (15 mg/kg) treated alone for 14 days in a row. Brain
homogenates were subjected to lead-induced changes in lipid peroxidation, nitric oxide, protein carbonyl, and
enzymatic and non-enzymatic activity levels. Examined were histological alterations in the cortex and hippocampal
regions. The findings showed that PbAc dramatically reduced glutathione content, superoxide dismutase, catalase,
glutathione peroxidase, and glutathione reducase activity while increasing hippocampus and cortical lipid
peroxidation and nitrite levels. In the hippocampus and cortex, histological examinations of lead-induced
neurotoxicity showed significant damage and a decrease in neuronal density. However, by reestablishing the
equilibrium between antioxidants and oxidants and improving motor coordination and memory function, esculin
therapy protected hippocampal and cortical neurons against PbAc-induced neurotoxicity. Additionally, esculin
reduces the amount of neuronal density and morphological damage in the C57bl/6 mice's cortex and hippocampus.
Therefore, the findings implies that esculin could be helpful in preventing neuronal damage caused by lead acetate.