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Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model
Li,Shuai1,2; Zhao,Xia1,2; Lazarovici,Philip3; Zheng,Wenhua1,2
2019
Source PublicationOxidative Medicine and Cellular Longevity
ISSN1942-0900
Volume2019
AbstractAlzheimer's disease is a severe neurodegenerative disease. Multiple factors involving neurofibrillary tangles and amyloid-β plaques lead to the progression of the AD, generated by aggregated hyperphosphorylated Tau protein. Inflammation, mitochondrial dysfunction, and oxidative stress play a significant role in the progression of AD. It has been therefore suggested that the multifactorial nature of AD pathogenesis requires the design of antioxidant drugs with a broad spectrum of neuroprotective activities. For this reason, the use of natural products, characterized by multiple pharmacological properties is advantageous as AD-modifying drugs over the single-targeted chemicals. Artemether, a peroxide sesquiterpenoid lipid-soluble compound, has been used in the clinic as an antimalarial drug. Also, it exhibits potent anti-inflammatory and antioxidant activities. Here, we report the neuroprotective effects of Artemether towards Aβ-induced neurotoxicity in neuronal cell cultures. A temporal correlation was found between Artemether neuroprotection towards Aβ-induced neurotoxicity and AMPK/GSK3β phosphorylation activity and increased expression of the activated Nrf2 signaling pathway. In 3xTg-AD mice, Artemether attenuated learning and memory deficits, inhibited cortical neuronal apoptosis and glial activation, inhibited oxidative stress through decrease of lipid peroxidation and increased expression of SOD, and reduced Aβ deposition and tau protein phosphorylation. Moreover, in 3xTg-AD mice, Artemether induced phosphorylation of the AMPK/GSK3β pathway which activated Nrf2, increasing the level of antioxidant protein HO-1. These activities probably produced the antioxidant and anti-inflammatory effects responsible for the neuroprotective effects of Artemether in the 3xTg-AD mouse model. These findings propose Artemether as a new drug for the treatment of AD disease.
DOI10.1155/2019/1862437
URLView the original
Language英語English
Scopus ID2-s2.0-85075996050
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Cited Times [WOS]:26   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionUniversity of Macau
Corresponding AuthorZheng,Wenhua
Affiliation1.Centre for Reproduction,Development and Aging,Faculty of Health Sciences,University of Macau,Taipa,Macao
2.Institute of Translational Medicine,Faculty of Health Sciences,University of Macau,Taipa,Macao
3.School of Pharmacy Institute for Drug Research,Faculty of Medicine,Hebrew University of Jerusalem,Jerusalem,91120,Israel
First Author AffilicationFaculty of Health Sciences
Corresponding Author AffilicationFaculty of Health Sciences
Recommended Citation
GB/T 7714
Li,Shuai,Zhao,Xia,Lazarovici,Philip,et al. Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model[J]. Oxidative Medicine and Cellular Longevity,2019,2019.
APA Li,Shuai,Zhao,Xia,Lazarovici,Philip,&Zheng,Wenhua.(2019).Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model.Oxidative Medicine and Cellular Longevity,2019.
MLA Li,Shuai,et al."Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model".Oxidative Medicine and Cellular Longevity 2019(2019).
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