Inhibitory Effect of Hexahydrocurcumin on Memory Impairment and Amyloidogenesis in Dexamethasone-Treated Mice.

Abstract

A high dose of dexamethasone induces neurodegeneration by initiating the inflammatory processes that lead to neural apoptosis. A dexamethasone administration model induces overproduction of amyloid-β (Aβ) and tau protein hyperphosphorylation and shows abnormalities of cholinergic function similar to Alzheimer's disease (AD). This study aimed to investigate the protective effect of hexahydrocurcumin on the brain of dexamethasone-induced mice. The results showed that hexahydrocurcumin and donepezil attenuated the levels of amyloid precursor protein and β-secretase mRNA by reverse transcription polymerase chain reaction, decreased the expression of hyperphosphorylated tau, and improved synaptic function. Moreover, we found that hexahydrocurcumin treatment could decrease interleukin-6 levels by attenuating p65 of nuclear factor kappa-light-chain-enhancer (NF-κB) of activated beta cells. In addition, hexahydrocurcumin also decreased oxidative stress, as demonstrated by the expression of 4-hydroxynonenal and thereby prevented apoptosis. Therefore, our finding suggests that hexahydrocurcumin prevents dexamethasone-induced AD-like pathology and improves memory impairment.