Abstract
The current work was aimed at evaluating the ameliorative role of quercetin (QR) on the possible toxicity of Red Bull energy drink (RB-Ed) in the cerebral cortex of rats. To achieve the goal, the rats were allocated into 4 groups. The first group received distilled water as control. Groups II and III were given Red Bull energy drink alone and in combination with quercetin, respectively. The fourth group served as recovery to group II. The experimental duration was four weeks for all groups whereas the recovery period of group IV was two weeks. QR upregulated the mRNA and protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) genes, which can protect against RB-Ed neurotoxicity. Moreover, by reducing the thiobarbituric acid reactive substance and increasing the total antioxidant capacity levels, QR protected rats' cerebral cortex against Red Bull energy drink-induced oxidative damage. Quercetin also inhibited RB-Ed-induced histomorphological degeneration which was confirmed by the increase in the intact neurons and the rise in the neuron-specific enolase immunoreaction. QR increased the reduction of the brain-derived neurotrophic factor that was elicited by RB-Ed and acts as an anti-inflammatory agent by reducing the proinflammatory marker, interleukin 1 beta and DNA damage markers, heat shock protein 70, and 8-hydroxydeoxyguanosine. It could be concluded that the alleviating impacts of QR on RB-Ed neurotoxicity in rats could be related to the modulation of Nrf2 and HO-1 which in turn affects the redox status.