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Deficiency of anti-inflammatory cytokine IL-4 leads to neural hyperexcitability and aggravates cerebral ischemia-reperfusion injury

Deficiency of anti-inflammatory cytokine IL-4 leads to neural hyperexcitability and aggravates cerebral ischemia-reperfusion injury

作     者:Xiaoling Chen Jingliang Zhang Yan Song Pan Yang Yang Yang Zhuo Huang Kewei Wang Xiaoling Chen;Jingliang Zhang;Yan Song;Pan Yang;Yang Yang;Zhuo Huang;Kewei Wang

作者机构:Department of Molecular and Cellular PharmacologyState Key Laboratory of Natural and Biomimetic DrugsPeking University School of Pharmaceutical SciencesBeijing 100191China Department of PharmacologyQingdao University School of PharmacyQingdao 266021China Department of Medicinal Chemistry and Molecular PharmacologyPurdue University College of PharmacyWest LafayetteIN 47907USA Institute of Innovative DrugsQingdao University School of PharmacyQingdao 266021China 

出 版 物:《Acta Pharmaceutica Sinica B》 (药学学报(英文版))

年 卷 期:2020年第10卷第9期

页      面:1634-1645,1802页

核心收录:

学科分类:1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基  金:supported by research grants from the National Natural Science Foundation of China(81573410) the National Science and Technology Major Project(2018ZX09711001-004006,China) the Natural Sciences Foundation of Shandong Province(ZR2015QL008,China)awarded to Kewei Wang 

主  题:Anoxic depolarization IL-4 Ischemia-reperfusion injury Neuronal excitability Synaptic transmissions 

摘      要:Systematic administration of anti-inflammatory cytokine interleukin 4(IL-4)has been shown to improve recovery after cerebral ischemic ***,whether IL-4 affects neuronal excitability and how IL-4 improves ischemic injury remain largely *** we report the neuroprotective role of endogenous IL-4 in focal cerebral ischemia-repertusion(I/R)*** multi-electrode array(MEA)recordings,IL-4 reduces spontaneous firings and network activities of mouse primary cortical ***-4 mRNA and protein expressions are upregulated after I/R *** deletion of 11-4 gene aggravates I/R injury in vivo and exacerbates oxygen-glucose deprivation(OGD)injury in cortical ***,supplemental IL-4 protects 11-4-/-cortical neurons against OGD ***,cortical pyramidal and stellate neurons common for ischemic penumbra after I/R injury exhibit intrinsic hyperexcitability and enhanced excitatory synaptic transmissions in Il-4-/-***,upregulation of Nav1.1 channel,and downregulations of KCa3.1 channel and a6 subunit of GABAA receptors are detected in the cortical tissues and primary cortical neurons from Il-4-/-*** together,our findings demonstrate that IL-4 deficiency results in neural hyperexcitability and aggravates I/R injury,thus activation of IL-4 signaling may protect the brain against the development of permanent damage and help recover from ischemic injury after stroke.

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