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Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling
Xia Zhao1,2,3; Xiaosu Huang4; Chao Yang1,2; Yizhou Jiang1,2; Wenshu Zhou1,2; Zheng WH(鄭文華)1,2
2022
Source PublicationInternational Journal of Molecular Sciences
ISSN1422-0067
Volume2022Issue:23Pages:6354
Abstract
The abnormal immune response is an early change in the pathogenesis of Alzheimer’s
disease (AD). Microglial activation is a crucial regulator of the immune response, which contributes
to progressive neuronal injury by releasing neurotoxic products. Therefore, fifinding effective drugs to
regulate microglial homeostasis and neuroinflflammation has become a new AD treatment strategy.
Artemisinin has potent anti-inflflammatory and immune activities. However, it is unclear whether
Artemisinin contributes to the regulation of microglial activation, thereby improving AD pathology.
This study found that Artemisinin signifificantly reduced amyloid beta-peptide 1–42 (Aβ1–42)-induced
increases in nitric oxide and reactive oxygen species and inflflammatory factors in BV2 cells. In
addition, Artemisinin inhibited the migration of microglia and prevented the expansion of the
inflflammatory cascade. The mechanical studies showed Artemisinin inhibited neuroinflflammation
and exerted neuroprotective effects by regulating the Toll-like receptor 4 (TLR4)/Nuclear factor-kappa
B (NF-κB) signaling pathway. Similar results were obtained in AD model mice, in which Artemisinin
administration attenuated Aβ1–42-induced neuroinflflammation and neuronal injury, reversing spatial
learning and memory defificits. The anti-inflflammatory effect of Artemisinin is also accompanied by
the activation of the TLR4/NF-κB signaling pathway in the animal model. Our results indicate that
Artemisinin attenuated Aβ1–42-induced neuroinflflammation and neuronal injury by stimulating the
TLR4/NF-κB signaling pathway. These fifindings suggest that Artemisinin is a potential therapeutic
agent for AD.
KeywordAlzheimer’s Disease Artemisinin Neuroinflammation Microglia Cognitive Disorder
DOI10.3390/ijms23116354
Language英語English
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Cited Times [WOS]:1   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionFaculty of Health Sciences
Corresponding AuthorXia Zhao
Affiliation1.Center of Reproduction, Development & Aging and Department of Pharmacology, Faculty of Health Sciences, University of Macau, Macau SAR 999078, China; yb77625@um.edu.mo (X.Z.); yb97634@um.edu.mo (C.Y.); yb77642@um.edu.mo (Y.J.); yb87618@um.edu.mo (W.Z.)
2.Institute of Translation Medicine, Faculty of Health Sciences, University of Macau, Macau SAR 999078, China
3.Hangzhou Medical College, Hangzhou 310000, China
4.School of Nursing, Guangdong Pharmaceutical University, Guangzhou 510006, China; 15915736152@163.com * Correspondence: wenhuazheng@um.edu.mo; Tel.: +853-88224919
First Author AffilicationFaculty of Health Sciences
Corresponding Author AffilicationFaculty of Health Sciences
Recommended Citation
GB/T 7714
Xia Zhao,Xiaosu Huang,Chao Yang,et al. Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling[J]. International Journal of Molecular Sciences,2022,2022(23):6354.
APA Xia Zhao,Xiaosu Huang,Chao Yang,Yizhou Jiang,Wenshu Zhou,&Zheng WH.(2022).Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling.International Journal of Molecular Sciences,2022(23),6354.
MLA Xia Zhao,et al."Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling".International Journal of Molecular Sciences 2022.23(2022):6354.
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