Scopoletin Ameliorates Lipopolysaccharide Induced Neuroinflammation, Oxidative Stress and Cognitive Dysfunction in Mice: A Mechanistic Study

Background: Alzheimer’s disease (AD), a progressive neuropsychiatric disorder, is characterized by neuroinflammation, β-amyloid plaques and neurofibrillary tangles. It has been demonstrated that systemic inflammation neuroinflammation caused lipopolysaccharide (LPS) injections in rodents leads to elevation Aβ levels neuronal cell death, finally resulting cognitive impairment.
 Methods: Animals received the experimental compound – Scopoletin (2.5, 5 or 10 mg/kg, i.p) for 31 days. Initially 14 days, they only drug; thereafter next 7 days LPS (0.25 mg/kg along with molecules.
 Treatment molecules was continued behavioural tests were performed. sacrificed on day 32 biochemical performed brain tissue homogenate.
 Results: administration improved memory cognition as indicated reduction of escape latency Morris water maze test increased number entries Y test. Malondialdehyde significantly after reduced glutathione, catalyse superoxide dismutase mice brains. scopoletin oxidative stress. Inflammatory markers. β-secretase apoptotic markers also markedly reduced.
 Conclusion: At medium high dose, showed promise response prophylactic entity induced neuroinflamation dysfunction model mice.