Electroacupuncture Ameliorates Neuroinflammation-Mediated Cognitive Deficits through Inhibition of NLRP3 in Presenilin1/2 Conditional Double Knockout Mice.
Electroacupuncture Ameliorates Neuroinflammation-Mediated Cognitive Deficits through Inhibition of NLRP3 in Presenilin1/2 Conditional Double Knockout Mice.
复制标题
电针通过抑制 Presenilin1/2 条件双敲除小鼠中的 NLRP3 改善神经炎症介导的认知缺陷。
DOI：
10.1155/2021/8814616
复制
发表时间：
2021
影响因子：
3.1
通讯作者：
Chen Y
中科院分区：
文献类型：
--
作者：
Li K;Shi G;Zhao Y;Chen Y;Gao J;Yao L;Zhao J;Li H;Xu Y;Chen Y
神经炎症被认为是促进阿尔茨海默病（AD）神经退行性变的重要发病机制之一。电针刺激作为一种补充和替代疗法，已广泛应用于临床抗炎治疗。然而，EA是否促进AD中神经炎症引起的认知缺陷仍不清楚。本研究以早老素1和早老素2条件性双基因敲除（PS cDKO）小鼠为研究对象，通过行为学、电生理和分子生物学分析，探讨电针百会、神庭穴的神经保护作用。首先，我们观察到EA改善记忆缺陷和受损的突触可塑性。此外，EA具有抑制PS cDKO小鼠中过度磷酸化的tau和稳健升高的NLRP 3、ASC、Caspase-1、IL-1β和IL-18的能力。重要的是，NLPR 3炎性体的有效和选择性抑制剂MCC 950在抑制PS cDKO小鼠的过度磷酸化tau和强烈升高的NLRP 3组分和神经炎症反应以及EA治疗方面具有相似的作用。此外，EA治疗不能与MCC 950施用组合进一步改善PS cDKO小鼠的AD样表型。因此，电针刺激GV 20和GV 24穴位可能是一种潜在的替代疗法，通过抑制NLRP 3炎性小体激活来阻止AD的认知缺陷。
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.
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DOI：
10.1155/2015/142129
发表时间：
2015
期刊：
Evidence-based complementary and alternative medicine : eCAM
影响因子：
--
作者：
Jiang J;Gao K;Zhou Y;Xu A;Shi S;Liu G;Li Z
通讯作者：
Li Z
影响因子：
168.9
作者：
Ballard, Clive;Gauthier, Serge;Jones, Emma
通讯作者：
Jones, Emma
影响因子：
64.8
作者：
通讯作者：
--
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DOI：
10.1155/2017/3435891
发表时间：
2017
期刊：
Evidence-based complementary and alternative medicine : eCAM
影响因子：
--
作者：
Ding N;Jiang J;Lu M;Hu J;Xu Y;Liu X;Li Z
通讯作者：
Li Z
影响因子：
158.5
作者：
in 't Veld, BA;Ruitenberg, A;Stricker, BHC
通讯作者：
Stricker, BHC