Lycium barbarum glycopeptide protects neurons from amyloid-beta toxicity

Abstract Oligomeric amyloid-beta deposition within neurons and its associated neurotoxicity are among the most direct indicators of the onset of Alzheimer’s disease. Investigations into strategies aimed at reducing amyloid-beta accumulation or promoting its clearance in neurons are currently being carried out. Lycium barbarum glycopeptide is rich in biologically active compounds and possesses antioxidant, anti-inflammatory, and neuroprotective properties. This study verified that the oligomer amyloid-beta1–42 induced toxic effects in mouse N2a neuroblastoma cells, resulting in elevated levels of reactive oxygen species and increased expression of the inflammatory enzyme inducible nitric oxide synthase. Lycium barbarum glycopeptide counteracted these effects by alleviating cell damage, enhancing cell viability, reducing the levels of reactive oxygen species and inducible nitric oxide synthase expression, and up-regulating the mRNA levels of antioxidant enzymes, including superoxide dismutase 1, superoxide dismutase 2, and glutathione peroxidase 4. Lycium barbarum glycopeptide also activated the phosphoinositide 3-kinase/Akt/p70S6K signaling pathway and promoted the expression of brain-derived neurotrophic factor, thus exerting neuroprotective effects. These findings indicate that Lycium barbarum glycopeptide may be a promising candidate for the treatment of Alzheimer’s disease.