Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease that primarily develops in old age. The main clinical symptom of the disease is memory loss. Therefore, the treatment of learning and memory dysfunction is an important research direction for prevention and treatment of AD. Studies have shown that scopolamine hydrobromide (SCOP), sodium nitrite (NaNO2) and ethanol impair memory acquisition, memory consolidation and memory retrieval in mice, respectively. Safflower yellow (SY) can effectively improve the memory function of AD mice, but the specific mechanism needs further exploration. In the present study, mice were injected with SCOP, NaNO2 and 40% ethanol to establish models of memory acquisition, memory consolidation and memory retrieval impairment. This study investigated the mechanism of SY treatment of AD from the perspectives of oxidative stress, the cholinergic system, the CREB/BDNF/TrkB signaling pathway and synaptic protein expression. We conducted several studies that have shown that after SY treatment, the memory ability of three memory impairment mice models improved, the pathological changes in brain tissue were reduced, the activity of cholinergic system-related enzymes were changed, the level of oxidative stress in the brain of mice was reduced, and the CREB/BDNF/TrkB pathway was activated. In addition, SY can also upregulate the expression of synapse-associated proteins and exert neuroprotective effects.