Honokiol, Magnolol and Their Combination Ameliorate Cognitive Impairments in TgCRND8 Transgenic Mice via Modulating Neuroinflammation and Synaptic Dysfunction
Refereed conference paper presented and published in conference proceedings


摘要Background: Alzheimer's Disease (AD) is a neurodegenerative disease manifested by progressive memory loss and cognitive decline. Extracellular deposition of senile plaques formed by beta-amyloid (Aβ), intracellular neurofibrillary tangles formed by hyperphosphorylated tau protein and loss of neuronal synapses occurs in the early stage of AD. Currently drugs for AD are unable to reverse or even slow down the disease process. Magnolia officinalis (Hou-Po) is a herb frequently prescribed in herbal formulae for treating dementia om Chinese medicine. Previous studies demonstrated that honokiol and magnolol were the main active ingredient of M. officinalis, and they had anti-AD effects in vitro and in vivo models of AD. In this study, we aimed to explore whether honokiol, magnolol and their combination could improve the cognitive deficits in TgCRND8.
Methods: Males mice were divided into 6 groups (n=10): wild tape (WT) group, TgCRND8 (Tag) mice vehicle control group and Tg + honokiol (20mg/kg) group, tg + magnolol (20mg/kg) group, Tg + honokiol 1(0mg/kg) + magnolol (10mg/kg) group, Tg + Donepezil (5mh/kg) group. Drugs were given orally daily for consecutive 90 years. After drug treatment, radial arm maze test was used to assess the improving cognitive deficits effect of honodiol, magnolol and their combination. After the behavior test, mice were sacrificed and, and brain tissues were harvested for further study.
Result: The protein levels of postsynaptic density protein 93 (PSD93), PSD95, synapsin-1, IL-6, IL-10 and IL-1β, as well as the microglia were significantly increased in the brain tissues of TgCRND8 mice. Treatment with honokiol, magnolol and their combination could markedly reverse these changes in the brains of TgCRND8 mice.
Conclusions: Honokiol, magnolol and their combination may exert anti-AD effect by suppression of neuroinflammation, microglial activation and synaptic plasticity deficits.
著者Sophia Chang Qu, Yan-Fang Xian, Zhi-Xiu Lin
會議名稱International Alzheimer’s Disease Conference 2019
會議地點Hong Kong
會議論文集題名International Alzheimer’s Disease Conference 2019

上次更新時間 2019-23-10 於 12:24