Quercetin-loaded selenium nanoparticles inhibit amyloid-β aggregation and exhibit antioxidant activity

Abnormal aggregation of amyloid-beta (A beta) particles and oxidative stress are pathological hallmarks of Alzheimer's disease (AD). Quercetin (Que), a flavonoid antioxidant, has been widely used to inhibit A beta fibril formation and can potentially attenuate oxidative stress. However, poor aqueous solubility, extensive first-pass metabolism, and low permeability of the blood-brain barrier (BBB) limit its clinical application. Herein, we introduce a simple strategy to develop nanocomposites (NC) for drug delivery. This method involves combining Que and Na2SeO3 to obtain selenium nanoparticles. These nanoparticles are then modified using a combination of acacia and polysorbate 80 (P80-Que@Se NC). This recently developed nanocomposite has the potential to enhance drug delivery across the blood-brain barrier (BBB) and polysorbate 80 act as a pharmaceutical excipient that increases the aqueous solubility of Que. In vitro results demonstrated that P80-Que@Se had high aqueous solubility compared to individual Que, and could effectively inhibit A beta fibrillation. In vitro Cell Counting Kit (CCK)-8 analysis indicated that P80-Que@Se nanocomposites could protect PC12 cells from H2O2 -induced cell death. Additionally, P80-Que@Se had high 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity and exhibited excellent antioxidant activity. This study suggested that P80-Que@Se NCs may aid in the treatment of AD and have broad implications for future NC-based studies and applications. In brief, we believe that this reliable drug delivery method will serve as a useful template for researchers designing therapies to be delivered across the BBB.