[1]任大斌　郑　平　冯九庚　段　剑　邹树峰　洪　涛　赵　麟　陈　伟.抑制ERK1/2对大鼠脑缺血再灌注损伤的保护作用[J].中国临床神经外科杂志,2019,(05):295-298.[doi:10.13798/j.issn.1009-153X.2019.05.012]
　REN Da-bin,ZHENG Ping,FENG Jiu-geng,et al.Protective effetc of inhbition of ERK1/2 on rats after cerebral ischemia-repufusion injury[J].,2019,(05):295-298.[doi:10.13798/j.issn.1009-153X.2019.05.012]
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抑制ERK1/2对大鼠脑缺血再灌注损伤的保护作用()
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《中国临床神经外科杂志》[ISSN:1009-153X/CN:42-1603/TN]

卷:
期数:
2019年05期
页码:
295-298
栏目:
论著
出版日期:
2019-05-27

文章信息/Info

Title:
Protective effetc of inhbition of ERK1/2 on rats after cerebral ischemia-repufusion injury
文章编号:
1009-153X（2019）05-0295-04
作者:
任大斌　郑　平　冯九庚　段　剑　邹树峰　洪　涛　赵　麟　陈　伟
201299 上海，上海健康医学院附属上海浦东新区人民医院神经外科（任大斌、郑　平、陈　伟）；330008 南昌， 南昌大学第一附属医院神经外科（冯九庚、段剑、邹树峰、洪　涛、陈　伟）；210029 南京，南京医科大学第一附属医院神经外科（赵　麟）
Author(s):
REN Da-bin1;  ZHENG Ping1;  FENG Jiu-geng2;  DUAN Jian2;  ZOU Shu-feng2;  Hong Tao2;  ZHAO Lin3;  CHEN Wei1; 2
1. Department of Neurosurgery, Affiliated People's Hospital of Shanghai Pudong New Area, Shanghai College of Medicine and Health Sciences, Shanghai 201299, China; 2. Department of Neurosurgery, The First Affliated Hospital of Nanchang University, Nanchang 330008, China; 3. Department of Neurosurgery, The First Affiliated Hospital, Nanjing Medical University, Nanjing 210009, China
关键词:
脑缺血再灌注损伤; 缝隙连接蛋白43; 缝隙连接蛋白40; 异型连接; 核因子-κB; 细胞外调节蛋白激酶; 大鼠
Keywords:
Ischemia reperfusion injury;  Cx43;  Cx40;  Heterotypic gap junction;  Nuclear factor-κB;  Rat
分类号:
R 743
DOI:
10.13798/j.issn.1009-153X.2019.05.012
文献标志码:
A
摘要:
目的 探讨抑制细胞外调节蛋白激酶（ERK）1/2对脑缺血再灌注（I/R）损伤大鼠的作用及对缝隙连接蛋白（Cx）40/Cx43异型缝隙连接表达以及核因子-κB（NF-κB）相关炎症因子p-IκBa、肿瘤坏死因子（TNF）-α及干扰素（IFN）表达的影响。方法 选取成年雄性100只大鼠随机分为5组，每组20只：假手术组（仅暴露双侧颈总动脉而不夹闭）；治疗组4 h组和治疗组8 h组（I/R后立即腹腔注射ERK1/2特异性抑制剂SCH772984，25 mg/kg）；④溶媒组（I/R后立即腹腔注射溶媒二甲基亚枫）；⑤模型组（阻断双侧颈总动脉血流30 min后，恢复血流，产生I/R损伤）。采用神经功能损伤程度量表（NSS）评分评估大鼠神经功能。采用干湿重法测定脑组织含水率。采用免疫印迹法测定损伤侧海马区皮质p-IκBa、TNF-α及IFN的表达，采用免疫共沉淀法检测Cx40/Cx43异型连接表达。结果 模型组NSS评分脑含水率、p-IκBa、TNF-α、IFN及Cx40/Cx43异型连接的表达水平较假手术组均明显增高（P<0.05），SCH772984干预后，均明显下降（P<0.05）。结论 抑制ERK1/2途径，可明显抑制Cx40/Cx43异型连接和NF-κB，减少炎症因子，缓解脑水肿，从而改善大鼠神经功能。
Abstract:
ObjectiveToinvestigatetheeffectofinhibitionofextracellularregulatedproteinkinase(ERK）1/2onratsafterthecerebralischemia-repufusion(I/R)injury.MethodsOnehundredadultSDratswererandomlydividedinto5groups20animalseach,i.e.shamoperation;treatmentgroups1and2inwhichtheanimalsreceivedtheintraperitonealinjectionofERK1/2inhibitorSCH772984(25mg/kg)immediatelyafterI/Randthenweresacrificed4and8hoursafterI/R,respectively;vehiclegroupinwhichtheanimalsreceivedintraperitonealinjectionofisovolumeticDMSOandthenweresacrificed8hoursafterI/R;injurygroupinwhichtheanimalswithoutreceivinganytreatmentweresacrificed8hoursafterI/R.ThecerebralI/Rinjurymodelwasestablishedbyclippingbilateralcommoncarotidarteries.ThecerebralwatercontentwasmeasuredbyHatashitawet-weightmethodin10ratsofeachgroup.Thelevelsofp-IκBa,tumornecrosisfactor-α(TNF-α),interferon(IFN)andCx40/Cx43heterotypicgapjunctionexpressionsweredeterminedinthehippocampaltissuesof10ratsofeachgroupbywesternblotandco-immunoprecipitation,respectively.ResultsWatercontentandlevelsofp-IκBa,TNF-α,IFNandCx40/Cx43heterotypicgapjunctionexpressionsweresignificantlylowerinthetreatmentgroups1and2thanthoseinthevehicleandinjurygroups(P<0.05)andweresignificantlyhigherthanthoseintheshamgroup(P<0.05).Therewerenosignificantlydifferencesinthecerebralwatercontentandthelevelsofp-IκBa,TNF-a,IFNandCx40/Cx43heterotypicgapjunctionexpressionsbetweenboththetreatmentgroups(P>0.05).ConclusionInhibitionofERK1/2mayrelievethecerebraloedemaandimprovetheneurologicalfunctionwhichmaybebydown-regulationofCx40/Cx43heterotypicgapjunctionandp-IκBaproteinexpressions,thenreducingthelevelsofinflammatoryfactorssuchasTNF-αandINFexpressionsintheratsafterI/Rinjury.

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备注/Memo

备注/Memo:
基金项目：上海健康医学院种子基金项目（SFP-18-21-13-007，SFP-18-21-13-005）；上海市浦东新区科委民生项目（PKJ2016-Y31)；国家自然科学基金（81701231）；上海市自然科学基金（16ZR1431500）
通讯作者：陈　伟，E-mail：22248223@qq.com
更新日期/Last Update: 2019-05-27