Neuroprotective effect of 1-Deoxynojirimycin on cognitive impairment, β-amyloid deposition, and neuroinflammation in the SAMP8 mice.

β-amyloid deposition and neuroinflammation play a crucial part in Alzheimer's disease. Therefore, this study was designed to find the effects of 1-deoxynojirimycin (DNJ) purified from mulberry leaves on pathological deposition of Aβ peptides and neuroinflammation in senescence-accelerated-prone mouse 8 (SAMP8) mice. Compared to senescence-accelerated-resistant mouse 1 (SAMR1) mice, SAMP8 mice exhibited conspicuous declines in spatial memory abilities and brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptors (TrkB) level in hippocampus; increased Aβ deposition, β-secretase (BACE1) level, microglia activation and inflammatory factors, including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) in the brain. The SAMP8 mice were treated with DNJ (40 or 160 mg/kg/day) by oral administration for two months. Our results indicated that DNJ treatment improved these changes, and the 160-mg/kg/day DNJ group revealed more significant alleviation. Therefore, DNJ potentially has the neuroprotective effect by inhibiting BACE1 expression, attenuating Aβ deposition, remitting neuroinflammation, and up-regulating the BDNF/TrkB signal pathway in the brain.