Alzheimer's disease (AD) affects people worldwide and is caused by chronic and progressive damage to the central nervous system. Lycium barbarum (LB), a renowned functional food and medicinal plant in Southeast Asia, may possess protective effects against nerve injury. The present study aimed to investigate the neuroprotective effects of LB water extract in a differentiated (D)PC12 cellular apoptosis model induced by L‑glutamic acid (L‑Glu), and a mouse model of AD, induced by the combination of AlCl3 and D‑galactose. LB markedly increased DPC12 cell survival against L‑Glu induced damage by increasing cell viability, reducing the apoptosis rate and G1 phase arrest, suppressing intracellular reactive oxygen species accumulation, blocking Ca2+ overload and preventing mitochondrial membrane potential depolarization. LB additionally normalized the expression levels of apoptosis regulator Bcl‑2, apoptosis regulator BAX, and cleaved caspase‑3, ‑8 and ‑9 in L‑Glu exposed cells. In the AD mouse model, LB increased the amount of horizontal and vertical movement in the autonomic activity test, improved endurance time in the rotarod test and decreased escape latency time in the Morris water maze test. Additionally, the levels of acetylcholine and choline acetyltransferase were significantly increased in the serum and hypothalamus in the LB‑treated AD mice. These data suggested that LB may exert neuroprotective effects and may aid in preventing neurodegenerative disease.
Keywords: Lycium barbarum; neuroprotection; apoptosis; Alzheimer's disease; mitochondria.