Abstract
Quercetin (QE), the major bioflavonoid in the human diet, has been reported to have many benefits and medicinal properties. However, its protective effects against lead (Pb)-induced neurotoxicity have not been clarified. The aim of the present study was to investigate the effects of QE on neurotoxicity in mice exposed to Pb. Mice were exposed to lead acetate (20 mg/kg body weight/day) intragastrically with or without QE (15 and 30 mg/kg body weight/day) coadministration for 3 months. The data showed that QE significantly prevented Pb-induced neurotoxicity in a dose-dependent manner. Exploration of the underlying mechanisms of QE action revealed that QE administration decreased Pb contents in blood (13.2, 19.1%) and brain (17.1, 20.0%). QE markedly increased NO production (39.1, 61.1%) and PKA activity (51.0, 57.8%) in brains of Pb-treated mice. Additionally, QE remarkably suppressed Pb-induced oxidative stress in mouse brain. Western blot analysis showed that QE increased the phosphorylations of Akt, CaMKII nNOS, eNOS, and CREB in brains of Pb-treated mice. The results suggest that QE can inhibit Pb-induced neurotoxicity and partly restore PKA, Akt, NOS, CaMKII, and CREB activities.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
