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

• المؤلفون الرئيسيون: Pranglada Jearjaroen, Kanet Pakdeepak, Chainarong Tocharus, Waraluck Chaichompoo, Apichart Suksamrarn, Jiraporn Tocharus
• التنسيق: دورية
• منشور في: 2020
• الموضوعات: Neuroscience; Pharmacology, Toxicology and Pharmaceutics
• الوصول للمادة أونلاين: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85089981333&origin=inward; http://cmuir.cmu.ac.th/jspui/handle/6653943832/70984
• المؤسسة: Chiang Mai University

© 2020, Springer Science+Business Media, LLC, part of Springer Nature. 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.