Protective Effect of Esculin Against Lead-Induced Brain Oxidative Stress in C57BL/6 Mice

Abstract

Due to oxidative stress caused by reactive oxygen species, heavy metal exposure to lead is linked to significant neuronal damage. This
research examined esculin's possible neuroprotective effects using the C57bl/6 model of lead (Pb)-induced brain damage. The research
used four mouse groups: 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 used to detect changes brought on by lead in the levels of lipid
peroxidation, nitric oxide, protein carbonyl, and enzymatic and non-enzymatic activity. Additionally, histological alterations in the
cortex and hippocampal regions were investigated. The findings showed that PbAc dramatically reduced glutathione content, superoxide
dismutase, catalase, glutathione peroxidase, and glutathione reductase activity while increasing nitrite and hippocampus and cortical
lipid peroxidation levels. The hippocampus and cortex showed significant damage and a decrease in neuronal density, according to
histological findings of lead-induced neurotoxicity. However, by reestablishing the equilibrium between oxidants and antioxidants,
esculin therapy saved hippocampal and cortical neurons from PbAc-induced neurotoxicity and improved memory and motor
coordination. Esculin also reduces the amount of neuronal density and morphological damage in the C57bl/6 mice's brain and
hippocampus. Esculin may thus be helpful in preventing lead acetate-induced neuronal damage, according to the research.