文献类型：期刊文献

中文题名：电头针对缺血性脑卒中大鼠缺血皮质区炎性反应及小胶质细胞极化的影响

英文题名：Effects of electro-scalp acupuncture on inflammatory response and microglial polarization in the ischemic cortex of rats with ischemic stroke

作者：彭晓云[1];袁博[2];田甜[3];罗文君[3];朱玲桂[3];张延菊[3];李颖[3];杜小正[4];王金海[3]

第一作者：彭晓云

机构：[1]兰州大学第二医院康复医学科,甘肃兰州730030;[2]甘肃中医药大学附属医院针灸临床中心;[3]兰州大学第二医院中医科,甘肃兰州730030;[4]甘肃中医药大学针灸推拿学院

第一机构：兰州大学第二医院康复医学科,甘肃兰州730030

年份：2023

卷号：43

期号：9

起止页码：1050

中文期刊名：中国针灸

外文期刊名：Chinese Acupuncture & Moxibustion

收录：CSTPCD;;Scopus;北大核心:【北大核心2020】；CSCD:【CSCD2023_2024】；PubMed;

基金：国家自然科学基金资助项目: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:gzfy-2019-13。

语种：中文

中文关键词：缺血性脑卒中;电头针;神经功能;小胶质细胞;炎性反应

外文关键词：ischemic stroke;electro-scalp acupuncture;neurological function;microglia;inflammatory response

摘要：目的:观察电头针对缺血性脑卒中大鼠缺血皮质区小胶质细胞标志物CD206、CD32及白细胞介素(IL)-6、IL-1β、IL-10表达的影响,探讨电头针缓解缺血性脑卒中炎性损伤的机制。方法:从60只7周龄雄性SD大鼠中随机选取15只作为假手术组,剩余大鼠采用线栓法复制大脑中动脉栓塞(MCAO)模型,将造模成功大鼠随机分为模型组、VitD3组和电头针组,每组15只。电头针组取双侧“顶颞前斜线”进行电针干预,疏密波,频率2 Hz/100 Hz,电流强度1 mA,每次30 min,每日1次,共7 d。VitD3组给予1,25-二羟维生素D3(1,25-VitD3)溶液(3 ng/100 g)灌胃,每日1次,共7 d。干预前和干预结束后,观察各组大鼠神经功能缺损评分及神经行为学评分。干预结束后,采用2,3,5-氯化三苯基四氮唑(TTC)染色法检测大鼠脑梗死体积;免疫荧光法检测大鼠缺血皮质区CD32和CD206蛋白表达;Western blot法检测大鼠缺血皮质区IL-6、IL-1β、IL-10蛋白表达。结果:与假手术组比较,模型组神经功能缺损评分和神经行为学评分升高(P<0.01),脑梗死体积增加(P<0.01),缺血皮质区CD32、IL-6、IL-1β蛋白表达增加(P<0.01),缺血皮质区CD206、IL-10蛋白表达减少(P<0.01)。与模型组比较,电头针组和VitD3组神经功能缺损评分和神经行为学评分降低(P<0.01),脑梗死体积缩小(P<0.01),缺血皮质区CD32、IL-6、IL-1β蛋白表达减少(P<0.01),缺血皮质区CD206、IL-10蛋白表达增加(P<0.01)。电头针组神经功能缺损评分低于VitD3组(P<0.05),脑梗死体积大于VitD3组(P<0.05),缺血皮质区CD32、CD206、IL-1β、IL-10蛋白表达少于VitD3组(P<0.01,P<0.05)。结论:电头针可改善MCAO模型大鼠神经功能,其机制可能与促进小胶质细胞M1型向M2型极化,缓解炎性损伤有关。
Objective To observe the effects of electro-scalp acupuncture(ESA)on the expression of microglial markers CD206 and CD32,as well as interleukin(IL)-6,IL-1β,and IL-10 in the ischemic cortex of rats with ischemic stroke,and to explore the mechanisms of ESA on alleviating inflammatory damage of ischemic stroke.Methods Sixty 7-week-old male SD rats were randomly selected,with 15 rats assigned to a sham surgery group.The remaining rats were treated with suture method to establish rat model of middle cerebral artery occlusion(MCAO).The rats with successful model were randomly divided into a model group,a VitD3 group,and an ESA group,with 15 rats in each group.In the ESA group,ESA was performed bilaterally at the"top-temporal anterior oblique line"with disperse-dense wave,a frequency of 2 Hz/100 Hz,and an intensity of 1 mA.Each session lasted for 30 min,once daily,for a total of 7 days.The VitD3 group were treated with intragastric administration of 1,25-dihydroxyvitamin D3(1,25-VitD3)solution(3 ng/100 g),once daily for 7 days.The neurological deficit scores and neurobehavioral scores were assessed before and after the intervention.After the intervention,the brain infarct volume was evaluated using 2,3,5-triphenyltetrazolium chloride(TTC)staining.Immunofluorescence double staining was performed to detect the protein expression of CD32 and CD206 in the ischemic cortex.Western blot analysis was conducted to measure the protein expression of IL-6,IL-1β,and IL-10 in the ischemic cortex.Results Compared with the sham surgery group,the model group showed increased neurological deficit scores and neurobehavioral scores(P<0.01),increased brain infarct volume(P<0.01),increased protein expression of CD32,IL-6,and IL-1βin the ischemic cortex(P<0.01),and decreased protein expression of CD206 and IL-10 in the ischemic cortex(P<0.01).Compared with the model group,both the ESA group and the VitD3 group showed decreased neurological deficit scores and neurobehavioral scores(P<0.01),reduced brain infarct volume(P<0.01),decreased protein expression of CD32,IL-6,and IL-1βin the ischemic cortex(P<0.01),and increased protein expression of CD206 and IL-10 in the ischemic cortex(P<0.01).Compared with the VitD3 group,the ESA group had lower neurological deficit score(P<0.05),larger brain infarct volume(P<0.05),and lower protein expression of CD32,CD206,IL-1β,and IL-10 in the ischemic cortex(P<0.01,P<0.05).Conclusion ESA could improve neurological function in MCAO rats,and its mechanism may be related to promoting microglial M1-to-M2 polarization and alleviating inflammatory damage.