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دسته بندی:
شبکه های نورونی - neuron-networks
سال انتشار:
2020
عنوان انگلیسی مقاله:
Deficiency of anti-inflammatory cytokine IL-4 leads to neural hyperexcitability and aggravates cerebral ischemia–reperfusion injury
ترجمه فارسی عنوان مقاله:
کمبود سیتوکین ضد التهاب IL-4 منجر به فشار بیش از حد عصبی شده و آسیب به ایسکمی مغزی - مجدد جریان خون را تشدید می کند.
منبع:
Sciencedirect - Elsevier - Acta Pharmaceutica Sinica B, Journal Pre-proof. doi:10.1016/j.apsb.2020.05.002
نویسنده:
Xiaoling Chen, Jingliang Zhang, Yan Song, Pan Yang, Yang Yang, Zhuo Huang, Kewei Wang
چکیده انگلیسی:
Systematic administration of anti-inflammatory cytokine interleukin 4 (IL-4) has been
shown to improve recovery after cerebral ischemic stroke. However, whether IL-4 affects
neuronal excitability and how IL-4 improves ischemic injury remain largely unknown. Here we
report the neuroprotective role of endogenous IL-4 in focal cerebral ischemia–reperfusion (I/R)
injury. In multi-electrode array (MEA) recordings, IL-4 reduces spontaneous firings and network
activities of mouse primary cortical neurons. IL-4 mRNA and protein expressions are
upregulated after I/R injury. Genetic deletion of Il-4 gene aggravates I/R injury in vivo and
exacerbates oxygen-glucose deprivation (OGD) injury in cortical neurons. Conversely,
supplemental IL-4 protects Il-4–/– cortical neurons against OGD injury. Mechanistically, cortical
pyramidal and stellate neurons common for ischemic penumbra after I/R injury exhibit intrinsic
hyperexcitability and enhanced excitatory synaptic transmissions in Il-4–/– mice. Furthermore, upregulation of Nav1.1 channel, and downregulations of KCa3.1 channel and α6 subunit of GABAA receptors are detected in the cortical tissues and primary cortical neurons from Il-4–/–
mice. Taken together, our findings demonstrate that IL-4 deficiency results in neural
hhoottppaappeerr..nneett 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.
KEY WORDS Anoxic depolarization | IL-4 | Ischemia–reperfusion injury | Neuronal excitability | Synaptic transmissions
قیمت: رایگان
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