LAUSR

BACKGROUND Neuroinflammation and oxidative stress have important effects on cognitive functions in the pathophysiological process of Alzheimer's disease (AD). In the current study, we determined the effects of Ampelopsin (AMP) on the levels of proinflammatory cytokines (PICs, IL-1β, IL-6 and TNF-α), and products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, a product of oxidative stress); and 8-hydroxy-2'-deoxyguanosine (8-OHdG, a key biomarker of protein oxidation) in the hippocampus using a rat model of AD. METHODS ELISA was used to examine PICs and products of oxidative stress; and western blot analysis was used to examine protein expression of NADPH oxidase (NOXs). The Spatial working memory tests and Morris water maze were used to assess cognitive functions. RESULTS We observed amplification of IL-1β, IL-6 and TNF-α as well as 8-iso PGF2α and 8-OHdG in the hippocampus of AD rats. Systemic administration of AMP attenuated upregulation of PICs and products of oxidative stress. AMP also inhibited NOX4 in the hippocampus of AD rats. Notably, AMP largely recovered the impaired learning performance in AD rat and this was linked to signal pathways of PIC and oxidative stress. CONCLUSION We showed the significant role of AMP in improving the memory impairment in AD rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress suggesting that AMP may present prospects in preventing and/or alleviating development of the impaired cognitive functions in AD as a complementary alternative intervention.