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CaMKIIα Signaling Is Required for the Neuroprotective Effects of Dl-3-n-Butylphthalide in Alzheimer's Disease.

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收录情况： ◇ SCIE

作者：
Li Bing-Qiu[1,2,3,4,5] * ; Xu Ling-Zhi[1,2,3,4,5] * ; Li Fang-Yu[1,2,3,4,5] ; Li Ying[1,2,3,4,5] ; Zhao Yu[5,6] ; Zhang Heng[1,2,3,4,5] ; Quan Mei-Na[1,2,3,4,5] ; Jia Jian-Ping[7,8,9,10,11] ;
机构： [1]Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Changchun Street 45, Xicheng District, Beijing, People’s Republic of China 100053 [2]Beijing Key Laboratory of Geriatric Cognitive Disorders, Beijing, People’s Republic of China [3]Clinical Center for Neurodegenerative Disease and Memory Impairment, Capital Medical University, Beijing, People’s Republic of China [4]Center of Alzheimer’s Disease, Collaborative Innovation Center for Brain Disorders, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, People’s Republic of China [5]Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing, People’s Republic of China [6]Cell Therapy Center, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing, People’s Republic of China
出处：
DOI： 10.1007/s12035-022-02777-8
ISSN：

关键词： Alzheimer’s disease DL-3-n-butylphthalide Neuroprotective effect CaMKIIα signaling

摘要：
Alzheimer's disease (AD) is the most common form of neurodegenerative disease and most anti-AD drugs have failed in clinical trials; hence, it is urgent to find potentially effective drugs against AD. DL-3-n-butylphthalide (NBP) is a compound extracted from celery seed and is a multiple-target drug. Several studies have demonstrated the neuroprotective effects of NBP on cognitive impairment, but the mechanisms of NBP remains relatively unexplored. In this study, we found that NBP could alleviated the increase of intracellular Ca2+ and reversed down-regulation of Ca2+/calmodulin-dependent protein kinase alpha (CaMKIIα) signaling and rescued neuronal apoptosis in SH-SY5Y cells treated by Aβ oligomers. However, these neuroprotective effects of NBP on neuronal damage and CaMKIIα signaling were abolished when CaMKIIα expression was knocked down or its activity was inhibited. Thus, our findings suggested that CaMKIIα signaling was required for the neuroprotective effects of NBP in AD and provided an improved basis for elucidating the mechanism and treatment of NBP in AD.© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

基金：
This study was supported by the National Natural Science Foundation of China (81801048), the Beijing Hospitals Authority Youth Programme (QMS20200805), the Youth Elite Scientists Sponsorship Program by CAST (YESS20200155), the Beijing Municipal Natural Science Foundation (7184215), the Key Project of the National Natural Science Foundation of China (81530036), the National Key Scientific Instrument and Equipment Development Project (31627803), the Key Project of the National Natural Science Foundation of China (U20A20354), the Beijing Scholars Program, and the Beijing Brain Initiative from Beijing Municipal Science & Technology Commission (Z201100005520016, Z201100005520017).
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外文
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出版当年[2021]版：
大类 | 2 区 医学
小类 | 2 区 神经科学
最新[2023]版：
大类 | 2 区 医学
小类 | 2 区 神经科学
JCR分区：
出版当年[2020]版：
Q1 NEUROSCIENCES
最新[2023]版：
Q1 NEUROSCIENCES

影响因子： 最新[2023版] 最新五年平均 出版当年[2020版] 出版当年五年平均 出版前一年[2019版] 出版后一年[2021版]

第一作者：
第一作者机构： [1]Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Changchun Street 45, Xicheng District, Beijing, People’s Republic of China 100053 [2]Beijing Key Laboratory of Geriatric Cognitive Disorders, Beijing, People’s Republic of China [3]Clinical Center for Neurodegenerative Disease and Memory Impairment, Capital Medical University, Beijing, People’s Republic of China [4]Center of Alzheimer’s Disease, Collaborative Innovation Center for Brain Disorders, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, People’s Republic of China [5]Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing, People’s Republic of China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Li Bing-Qiu,Xu Ling-Zhi,Li Fang-Yu,et al.CaMKIIα Signaling Is Required for the Neuroprotective Effects of Dl-3-n-Butylphthalide in Alzheimer's Disease.[J].MOLECULAR NEUROBIOLOGY.2022,59(6):3370-3381.doi:10.1007/s12035-022-02777-8.
APA：
Li Bing-Qiu,Xu Ling-Zhi,Li Fang-Yu,Li Ying,Zhao Yu...&Jia Jian-Ping.(2022).CaMKIIα Signaling Is Required for the Neuroprotective Effects of Dl-3-n-Butylphthalide in Alzheimer's Disease..MOLECULAR NEUROBIOLOGY,59,(6)
MLA：
Li Bing-Qiu,et al."CaMKIIα Signaling Is Required for the Neuroprotective Effects of Dl-3-n-Butylphthalide in Alzheimer's Disease.".MOLECULAR NEUROBIOLOGY 59..6(2022):3370-3381

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