详细信息
基于IFN-γ介导的JAK/STAT1信号通路探讨电头针缓解缺血性脑卒中大鼠神经炎性损伤的研究 被引量:2
Study on alleviating neuroinflammatory injury in ischemic stroke rats by electrical stimulation with scalp acupuncture based on IFN-γmediated JAK/STAT1 signaling pathway
文献类型:期刊文献
中文题名:基于IFN-γ介导的JAK/STAT1信号通路探讨电头针缓解缺血性脑卒中大鼠神经炎性损伤的研究
英文题名:Study on alleviating neuroinflammatory injury in ischemic stroke rats by electrical stimulation with scalp acupuncture based on IFN-γmediated JAK/STAT1 signaling pathway
作者:彭晓云[1];袁博[2];李兴兰[3];鲍英存[1];罗文君[4];张延菊[4];赵敏[4];王金海[4]
第一作者:彭晓云
机构:[1]兰州大学第二医院康复医学科,兰州730030;[2]甘肃中医药大学附属医院针灸临床中心,兰州730000;[3]甘肃中医药大学定西校区医学教学部,甘肃定西743000;[4]兰州大学第二医院中医科,兰州730030
第一机构:兰州大学第二医院康复医学科,兰州730030
年份:2023
卷号:48
期号:9
起止页码:852
中文期刊名:针刺研究
外文期刊名:Acupuncture Research
收录:CSTPCD;;Scopus;北大核心:【北大核心2020】;CSCD:【CSCD2023_2024】;PubMed;
基金:国家自然科学基金项目(No.81960896);甘肃中医药大学附属医院院内科研及技术创新基金青年项目(No.gzfy-2019-13)。
语种:中文
中文关键词:缺血性脑卒中;电头针;神经炎性损伤;Janus激酶/信号转导和转录激活因子1信号通路
外文关键词:Ischemic stroke;Electrical stimulation with scalp acupuncture;Neuroinflammatory injury;Janus kinase/signal transduction and activator of transcription 1 signaling pathway
摘要:目的:观察电头针对缺血性脑卒中(IS)大鼠缺血皮层区干扰素γ(IFN-γ)、Janus激酶/信号转导和转录激活因子1(JAK/STAT1)信号通路及炎性因子的影响,探讨其缓解IS大鼠神经炎性损伤的分子机制。方法:SD大鼠随机分为正常组、模型组、电头针组、抑制剂组,每组14只。采用线栓法复制大脑中动脉栓塞大鼠模型。抑制剂组腹腔注射抑制剂PJ34(25 mg/kg),1次/d,共7 d。电头针组取双侧“顶颞前斜线”予电头针干预,30 min/次,1次/d,共7 d。干预前和干预后,对各组大鼠行神经功能缺损评分及神经行为学评分;TTC染色法检测脑梗死体积;免疫组织化学法检测大鼠大脑皮层白细胞介素(IL)-6、IL-10的阳性表达;Western blot法检测大鼠大脑皮层IFN-γ、JAK1、JAK2和磷酸化(p)-STAT1蛋白的表达水平。结果:与正常组比较,模型组神经功能缺损评分和神经行为学评分明显升高(P<0.01),脑梗死体积明显增大(P<0.01),脑组织IL-6、IFN-γ、JAK1、JAK2、p-STAT1表达水平升高(P<0.01),IL-10表达水平降低(P<0.01)。与模型组比较,干预后抑制剂组和电头针组神经功能缺损评分和神经行为学评分明显降低(P<0.01),脑梗死体积减小(P<0.01),脑组织IL-6、IFN-γ、JAK1、JAK2、p-STAT1表达水平降低(P<0.01),IL-10表达水平升高(P<0.01)。电头针在改善神经功能缺损评分和下调p-STAT1的表达方面优于抑制剂(P<0.05,P<0.01),在改善脑梗死体积和下调IFN-γ、JAK1方面不及抑制剂(P<0.01,P<0.05)。结论:下调IFN-γ表达,进而抑制JAK/STAT1信号通路活性可能是电头针缓解IS神经炎性损伤的机制之一。
Objective To explore the molecular mechanism of electrical stimulation with scalp acupuncture(ESA)in alleviating neuroinflammatory injury in ischemic stroke rats based on interferonγ(IFN-γ)-mediated Janus ki?nase/signal transduction and transcriptional activator 1(JAK/STAT1)signaling pathway.Methods Fifty-six SD rats aged 7 weeks were randomly divided into normal,model,ESA and inhibitor groups,with 14 rats in each group.The middle cerebral artery embolization rat model was established by means of thread embolization.Rats in the inhibitor group were intraperitoneally injected with the inhibitor PJ34(5 mg/mL,25 mg/kg)once a day for 7 days.Rats in the ESA group were treated at bilateral anterior parietotemporal slash(MS6)with ESA(2 Hz/100 Hz,1 mA),30 min a day for 7 days.Before and after interventions,the neurological deficit score and neurobehavioral score were evaluated.The percentage of cerebral infarction volume was detected by TTC staining.The positive expressions of interleukin(IL)-6 and IL-10 in cerebral cortex were detected by immunohistochemistry.The protein expression levels of IFN-γ,JAK1,JAK2 and phosphorylated(p)-STAT1 in rats cerebral cortex were detected by Western blot.Results Compared with the normal group,the neurological deficit score,neurobehavioral score,the percentage of cerebral infarction volume,the expression levels of IL-6,IFN-γ,JAK1,JAK2 and p-STAT1 in cerebral cortex were increased(P<0.01),while the expression level of IL-10 was decreased(P<0.01)in the model group.Compared with the model group,the neurologi?cal deficit score and neurobehavioral score after treatment were significantly decreased(P<0.01),the percentage of ce?rebral infarction volume was decreased(P<0.01),the expression levels of IL-6,IFN-γ,JAK1,JAK2 and p-STAT1 in cerebral cortex were decreased(P<0.01),while the expression level of IL-10 was increased(P<0.01)in the ESA and inhibitor groups.ESA was superior to inhibitors in improving neurological deficit score and down-regulating p-STAT1 ex?pression(P<0.05,P<0.01),and was inferior to inhibitor in reducing the percentage of cerebral infarction volume as well as down-regulating IFN-γand JAK1(P<0.01,P<0.05).Conclusion Down-regulating the expression of IFN-γand in?hibiting the activity of JAK/STAT1 signaling pathway may be one of the mechanisms by which ESA alleviates neuroin?flammatory injury in ischemic stroke rats.
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