Quercetin mitigates scopolamine-induced memory dysfunction: impact on oxidative stress and cholinergic mechanisms.

Despite the promising neuroprotective activities of quercetin (QT), its' effect on cholinergic neurotransmission needs further elucidation. In this study, we explored the impact of QT on oxidative stress and cholinergic neurotransmission with emphasis on the possible involvement of choline acetyltransferase (ChAT) as a potential mechanism of QT on memory function at the hippocampal sub-regions and prefrontal cortex of mice brains. Mice were administered orally with QT (12.5 and 25 mg/kg) alone or in combination with SC (3 mg/kg, intraperitoneally) once daily for seven consecutive days. Thirty minutes after the last treatment, memory function was assessed using the Y-maze test. Levels of biomarkers of oxidative stress and acetylcholinesterase (AChE) activity were determined using a microplate reader. ChAT activity was determined by immunohistochemistry. QT pretreatment enhanced memory performance and reversed scopolamine (SC)-induced memory impairment in the Y-maze test. QT also reduced malondialdehyde and nitrite levels in mice brains. Glutathione levels were increased in mice brains as a result of QT administration. Levels of antioxidant enzymes (superoxide dismutase and catalase) were significantly increased in the mice brains, but AChE activity was reduced by QT. The activity of ChAT was significantly enhanced by QT in the hippocampal sub-regions and the prefrontal cortex of the mice brains. This study has shown that QT mitigated SC-induced memory dysfunction by inhibiting oxidative stress and AChE activity. Also, QT enhanced ChAT activity, particularly in the hippocampal sub-regions and the prefrontal cortex. These mechanisms, may be possible means through which QT improves memory performance.