Inhibitory Effect of Hexahydrocurcumin on Memory Impairment and Amyloidogenesis in Dexamethasone-Treated Mice
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ORIGINAL ARTICLE
Inhibitory Effect of Hexahydrocurcumin on Memory Impairment and Amyloidogenesis in Dexamethasone-Treated Mice Pranglada Jearjaroen 1 & Kanet Pakdeepak 1 & Chainarong Tocharus 2 & Waraluck Chaichompoo 3 & Apichart Suksamrarn 3 & Jiraporn Tocharus 1,4 Received: 28 June 2020 / Revised: 23 July 2020 / Accepted: 4 August 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
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-chainenhancer (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. Keywords Dexamethasone . Alzheimer’s disease . Amyloidogenesis . Hexahydrocurcumin . Donepezil
Introduction Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disease that is characterized by memory loss, learning impairment, and cognition deficit (Kumar et al. 2015). The incidence of AD is rapidly increasing and becoming a worldwide economic problem (Sosa-Ortiz et al.
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12640-020-00269-y) contains supplementary material, which is available to authorized users. * Jiraporn Tocharus [email protected] 1
Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
2
Department of Anatomy, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
3
Department of Chemistry and Center of Excellence for Innovation in Chemistry, Faculty of Science, Ramkhamhaeng University, Bangkok, Thailand
4
Center for Research and Development of Natural Products for Health, Chiang Mai University, Chiang Mai, Thailand
2012; Wimo et al. 2017). The pathology of AD is related to an increase in amyloid-β (Aβ) and hyperphosphorylation of the tau protein (Zheng et al. 2002). Aβ results from the sequential proteolysis of the amyloid precursor protein (APP) by the βsite APP-cleaving enzyme (BACE1) and γ-secretase, which forms senile plaques (Jarrett et al. 1993; LaFerla et al. 2007; Vassar et al. 1999). The accu
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