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Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling
Zhao, Xia1,2,3; Huang, Xiaosu4; Yang, Chao1,2; Jiang, Yizhou1,2; Zhou, Wenshu1,2; Zheng, Wenhua1,2
2022-06-01
Source PublicationInternational Journal of Molecular Sciences
ISSN1661-6596
Volume23Issue:11
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, finding effective drugs to regulate microglial homeostasis and neuroinflammation has become a new AD treatment strategy. Artemisinin has potent anti-inflammatory 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 significantly reduced amyloid beta-peptide 1–42 (Aβ)-induced increases in nitric oxide and reactive oxygen species and inflammatory factors in BV2 cells. In addition, Artemisinin inhibited the migration of microglia and prevented the expansion of the inflammatory cascade. The mechanical studies showed Artemisinin inhibited neuroinflammation 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 Aβ-induced neuroinflammation and neuronal injury, reversing spatial learning and memory deficits. The anti-inflammatory 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 Aβ-induced neuroinflammation and neuronal injury by stimulating the TLR4/NF-κB signaling pathway. These findings suggest that Artemisinin is a potential therapeutic agent for AD.

KeywordAlzheimer’s Disease Artemisinin Cognitive Disorder Microglia Neuroinflammation
DOI10.3390/ijms23116354
URLView the original
Indexed BySCIE
Language英語English
WOS Research AreaBiochemistry & Molecular Biology ; Chemistry
WOS SubjectBiochemistry & Molecular Biology ; Chemistry, Multidisciplinary
WOS IDWOS:000808635800001
Scopus ID2-s2.0-85131290572
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Document TypeJournal article
CollectionFaculty of Health Sciences
Corresponding AuthorZheng, Wenhua
Affiliation1.Center of Reproduction, Development & Aging and Department of Pharmacology, Faculty of Health Sciences, University of Macau, 999078, Macao
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
First Author AffilicationFaculty of Health Sciences
Corresponding Author AffilicationFaculty of Health Sciences
Recommended Citation
GB/T 7714
Zhao, Xia,Huang, Xiaosu,Yang, Chao,et al. Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling[J]. International Journal of Molecular Sciences,2022,23(11).
APA Zhao, Xia,Huang, Xiaosu,Yang, Chao,Jiang, Yizhou,Zhou, Wenshu,&Zheng, Wenhua.(2022).Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling.International Journal of Molecular Sciences,23(11).
MLA Zhao, Xia,et al."Artemisinin Attenuates Amyloid-Induced Brain Inflammation and Memory Impairments by Modulating TLR4/NF-κB Signaling".International Journal of Molecular Sciences 23.11(2022).
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