Ampelopsin Improves Cognitive Impairment in Alzheimer’s Disease and Effects of Inflammatory Cytokines and Oxidative Stress in the Hippocampus

Background: Neuroinflammation and oxidative stress have significant effects on cognitive deficiency in the pathophysiological development of Alzheimer’s disease (AD). In the present study, we studied the influences of Ampelopsin (AMP) on 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 oxidative stress production; and western blotting to examine NADPH oxidase (NOXs). The Spatial working memory tests and Morris water maze were utilized 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. AMP attenuated upregulation of PICs and oxidative stress production. AMP also inhibited NOX4 in the AD rat hippocampus. Notably, AMP mostly improved learning performance in AD rat and this was linked to signal pathways of PIC and oxidative stress. Conclusion: AMP plays a significant role in improving the memory deficiency in AD rats via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that AMP is likely to prospect in preventing and relieving development of the cognitive dysfunctions in AD as a complementary alternative intervention.