Electroacupuncture Ameliorates Neuroinflammation-Mediated Cognitive Deficits through Inhibition of NLRP3 in Presenilin1/2 Conditional Double Knockout Mice

Copyright © 2021 Kun Li et al.

Bibliographische Detailangaben
Veröffentlicht in:Neural plasticity. - 1998. - 2021(2021) vom: 15., Seite 8814616
1. Verfasser: Li, Kun (VerfasserIn)
Weitere Verfasser: Shi, Guoqi, Zhao, Yang, Chen, Yiwen, Gao, Jie, Yao, Lin, Zhao, Jiaying, Li, Hongzhu, Xu, Ying, Chen, Yongjun
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2021
Zugriff auf das übergeordnete Werk:Neural plasticity
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Furans Indenes Inflammation Mediators NLR Family, Pyrin Domain-Containing 3 Protein Nlrp3 protein, mouse Presenilin-1 Presenilin-2 Psen2 protein, mouse mehr... Sulfonamides presenilin 1, mouse N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide 6RS86E2BWQ
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245 1 0 |a Electroacupuncture Ameliorates Neuroinflammation-Mediated Cognitive Deficits through Inhibition of NLRP3 in Presenilin1/2 Conditional Double Knockout Mice 
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520 |a Copyright © 2021 Kun Li et al. 
520 |a Neuroinflammation is considered as one of the crucial pathogenesis in promoting neurodegenerative progress of Alzheimer's disease (AD). As complementary and alternative therapy, electroacupuncture (EA) stimulation has been widely used in clinical practice for anti-inflammation. However, whether EA promotes the cognitive deficits resulting from neuroinflammation in AD remains unclear. In this study, the presenilin 1 and 2 conditional double knockout (PS cDKO) mice, exhibited a series of AD-like pathology, robust neuroinflammatory responses, and memory deficits, were used to evaluate the potential neuroprotective effect of EA at Baihui (GV 20) and Shenting (GV 24) by behavioral testing, electrophysiology recording, and molecular biology analyzing. First, we observed that EA improved memory deficits and impaired synaptic plasticity. Moreover, EA possesses an ability to suppress the hyperphosphorylated tau and robust elevated NLRP3, ASC, Caspase-1, IL-1β, and IL-18 in PS cDKO mice. Importantly, MCC950, a potent and selective inhibitor of NLPR3 inflammasome, has similar effects on inhibiting the hyperphosphorylated tau and the robust elevated NLRP3 components and neuroinflammatory responses of PS cDKO mice as well as EA treatment. Furthermore, EA treatment is not able to further improve the AD-like phenotypes of PS cDKO mice in combination with the MCC950 administration. Therefore, EA stimulation at GV 20 and GV 24 acupoints may be a potential alternative therapy for deterring cognitive deficits in AD through suppression of NLRP3 inflammasome activation 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a Furans  |2 NLM 
650 7 |a Indenes  |2 NLM 
650 7 |a Inflammation Mediators  |2 NLM 
650 7 |a NLR Family, Pyrin Domain-Containing 3 Protein  |2 NLM 
650 7 |a Nlrp3 protein, mouse  |2 NLM 
650 7 |a Presenilin-1  |2 NLM 
650 7 |a Presenilin-2  |2 NLM 
650 7 |a Psen2 protein, mouse  |2 NLM 
650 7 |a Sulfonamides  |2 NLM 
650 7 |a presenilin 1, mouse  |2 NLM 
650 7 |a N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide  |2 NLM 
650 7 |a 6RS86E2BWQ  |2 NLM 
700 1 |a Shi, Guoqi  |e verfasserin  |4 aut 
700 1 |a Zhao, Yang  |e verfasserin  |4 aut 
700 1 |a Chen, Yiwen  |e verfasserin  |4 aut 
700 1 |a Gao, Jie  |e verfasserin  |4 aut 
700 1 |a Yao, Lin  |e verfasserin  |4 aut 
700 1 |a Zhao, Jiaying  |e verfasserin  |4 aut 
700 1 |a Li, Hongzhu  |e verfasserin  |4 aut 
700 1 |a Xu, Ying  |e verfasserin  |4 aut 
700 1 |a Chen, Yongjun  |e verfasserin  |4 aut 
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