Silymarin-Encapsulated Xanthan Gum–Stabilized Selenium Nanocarriers for Enhanced Activity Against Amyloid Fibril Cytotoxicity

The accumulation of amyloid-beta at the neuronal sites is a major pathological hallmark involved in the etiology of Alzheimer’s disease. To reduce the Aβ-induced neuronal cytotoxicity, selenium nanoparticles and silymarin were fabricated in a single polysaccharide matrix for dual antioxidant and Aβ fibril disaggregation activity. These nanoparticles were further stabilized by an exopolysaccharide xanthan gum. The nanoparticles were fabricated to reduce the amyloid-induced cytotoxicity in SH-SY5Y cells. A three-step method employing redox reaction of sodium selenite and ascorbic acid has been adopted for the synthesis of selenium nanoparticles. Consequently, xanthan gum powder was added to impart stability to the nanocarriers. The nanoparticles exhibited a particle size of 119.2 ± 2.8 nm, zeta potential of − 35.4 ± 3.8 mV, and % EE of 87.7 ± 2.23. HR-TEM with EDX analysis confirmed the presence of spherical nanoparticles. An in vitro drug release study exhibited 89.33 ± 5.4% release of silymarin from nanocarriers and was able to scavenge 90% free radicals of DPPH reagent. The thioflavin T (ThT) fibrillation kinetics study showed that the nanoparticles elicited maximum disaggregation of Aβ fibrils that was depicted by the quenched fluorescence intensity signal. The cell viability results revealed that the highest neuroprotection activity was observed in the cell group treated with SLY-XG-Se against Aβ 1–42 -induced toxicity. The nanoparticles were able to internalize in SH-SY5Y cells. Our findings showed that the nanocarrier elicited anti-aggregation efficacy in neuronal cell lines and mitigated the Aβ-induced cytotoxicity, which represents the prospects of neuroprotection involved in the therapeutics of AD. Graphical abstract