[1]王宏斌,郑新瑞,袁华,等.RIP1/3对创伤性脑损伤后神经元的作用及其机制研究[J].卒中与神经疾病杂志,2017,24(01):45-49+55.[doi:10.3969/j.issn.1007-0478.2017.01.012]
 Wang Hongbin,Zheng Xinrui,Yuan Hua,et al.The effect and mechanism of RIP1/3 on neurons after traumatic brain injury[J].Stroke and Nervous Diseases,2017,24(01):45-49+55.[doi:10.3969/j.issn.1007-0478.2017.01.012]
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RIP1/3对创伤性脑损伤后神经元的作用及其机制研究()
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第24卷
期数:
2017年01期
页码:
45-49+55
栏目:
论 著
出版日期:
2017-02-26

文章信息/Info

Title:
The effect and mechanism of RIP1/3 on neurons after traumatic brain injury
文章编号:
1007-0478(2017)01-0045-06
作者:
王宏斌郑新瑞袁华何芳梅
710032 西安,第四军医大学西京医院康复理疗科[王宏斌(共同第一作者,硕士在读)袁华(通讯作者)],神经外科 [郑新瑞(共同第一作者)]; 西安交通大学医学部研究生院康复与理疗专业[何芳梅]
Author(s):
Wang HongbinZheng XinruiYuan Huaet al.
Department of Rehabilitation and Physiotherapy,Xijing Hospital,The Fourth Military Medical University,Xi'an 710032
关键词:
创伤性脑损伤 受体相互作用蛋白1/3 神经元 谷氨酸
Keywords:
Traumatic brain injury RIP1/3 Neuron Glutamate
分类号:
R741
DOI:
10.3969/j.issn.1007-0478.2017.01.012
摘要:
目的 探讨RIP1/3对创伤性脑损伤(TBI)后神经元的影响及其作用机制。方法 将体外培养的皮层神经元分为4组:siRIP组、Nec-1预处理组、阴性质粒转染组和对照组。通过慢病毒转染法分别干涉RIP1、RIP3表达,建立离体TBI损伤模型,通过流式细胞学检测划伤后神经元存活情况。对体外培养的皮层神经元敲除RIP1/3,建立谷氨酸诱导神经元损伤模型,通过流式细胞学检测谷氨酸刺激后神经元存活情况。结果 siRIP组及Nec-1预处理组机械性损伤后神经元存活率高于阴性质粒转染组和对照组。Nec-1预处理组谷氨酸损伤后神经元存活率高于对照组,而siRIP组存活率与对照组和阴性转染组比较未见显著差异。结论 RIP1和RIP3可能对TBI诱导后神经元死亡有作用,而RIP1抑制剂Nec-1可能对TBI具有脑保护作用。RIP1/3与谷氨酸兴奋毒性诱导细胞死亡无关,而Nec-1对于谷氨酸损伤具有潜在保护作用,并可能存在特异性靶点。
Abstract:
ObjectiveTo investigate the effect and mechanism of RIP1/3 on neurons after traumatic brain injury(TBI).Methods The cultured cortical neurons were divided into four groups:siRIP group,Nec-1 pretreatment group,negative plasmid transfection group and control group.The TBI damage model was established by interfering with the expression of RIP1 and RIP3 through lentiviral transfection,respectively.The RIP3 damage model was established,and the survival rate of neurons was detected by flow cytometry.Results After mechanical injury,the survival rate of neurons in the siRIP group and in the Nec-1 pretreatment group was higher than that in the negative plasmid transfection group and in the control group.After glutamate stimulation,the survival rate of neurons in the Nec-1 pretreatment group was higher than that in the control group.siRIP3 group or siRIP1 group showed no significant difference in the survival rate of neurons when contrasted with the negative control transfection group.Conclusion RIP1 and RIP3 may play a role in neuronal death induced by TBI,RIP1 inhibitor Nec-1 may have a function in brain protection for TBI.RIP1 and RIP3 have no effect on neuron cell death induced by glutamate excitotoxicity.Nec-1 has a potential protective effect on glutamate injury,probably suggesting a specific target.

参考文献/References:

[1] Moretti L,Cristofori I,Weaver SM,et al.Cognitive decline in older adults with a history of traumatic brain injury[J].The Lancet Neurology,2012,11(12):1103-1112.
[2] Langlois JA,Rutland-Brown W,Wald MM.The epidemiology and impact of traumatic brain injury:a brief overview[J].J Head Trauma Rehabil,2006,21(5):375-378.
[3] Graham DI,Mcintosh TK,Maxwell WL,et al.Recent advaces in neurotrauma[J].J Neuropathol Exp Neurol,2000,59(8):641-651.
[4] Ai FD.O'leary DM,fan L,Bao W,mullins PG,movsesyan VA[J].Selective blockade of the mGluR1 trauma.Exp Neurol,2001,167(2):435-444.
[5] Huang WD,Fei Z,Zhang X.Traumatic injury induced homer-1a gene expression in cultured cortical neurons of rat[J].Neurosci Lett,2005,389(1):46-50.
[6] Rosonke S,Legome E.Head trauma[J].J emerg Med,2006,31(4):421-425.
[7] 费舟.现代颅脑损伤学[M].北京:人民军医出版社,2007.
[8] Federal Interagency Head Injury Task Force Report.Washington[Z],1989.
[9] Langlois JA,Rutland-Brown W,Tomas K.Traumatic brain injury in the United States:emergency department visits hospitalization and deaths[Z],2004.
[10] Thurman DJ,Alverson C,Dunn KA,et al.Traumatic brain injury in the United States:A public health perspective[J].J Head Trauma Rehabil,1999,14(6):602-615.
[11] Zhao YD,Wang W.Neurosurgical trauma in People's Republic of China[J].World J Surg,2001,25(9):1202-1204.
[12] Rink A,Fung KM,Trojanowski JQ,et al.Evidence of apoptosis cell death after experience traumatic brain injury in rat[J].Am J Pathol,1995,147(6):1575.
[13] Conti AC,Raghupathi R,Trojanowski JQ,et al.Experimental brain injury induces regionally distinct apoptosis during the acute and delayed post-traumatic period[J].J Neurosci,1998,18(15):5663-5672.
[14] Williams S,Raghupathi R,Mackinnon MA,et al.In situ DNA fragmentation occurs in white matter up to 12 months after head injury in man[J].Acta Neuropathol,2001,102(6):581-590.
[15] 雪亮,杨树源.人脑创伤后神经元凋亡及调节机制的观察[J].中华创伤杂志,2003,19(3):160-163.
[16] Degterev A,Huang ZH,Boyce M,et al.Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury[J].Nat Chem Biol,2005,1(2):112-119.
[17] Han WD,Xie JS,Li L,et al.Necrostatin-1 reverts shikonin-induced necroptosis to apoptosis[J].Apoptosis,2009,14(5):674-686.
[18] Xu X,Chua CC,Kong J,et al.Necrostatin-1 protects against glutamate-induced glutathione depletion and caspase-independent cell death in HT-22 cells[J].J Neurochem,2007,103(5):2004-2014.
[19] Xu X,Chua KW,Chua CC,et al.Synergistic protective effects of humanin and necrostatin-1 on hypoxia and ischemia/reperfusion injury[J].Brain Res,2010,1355(2):189-194.
[20] Rosenbaum DM,Degterev A,David J,et al.Necroptosis,a novel form of caspase-independent cell death,contributes to neuronal damage in a retinal ischemia-reperfusion injury model[J].J Neurosci Res,2010,88(7):1569-1576.
[21] Lin MT,Beal MF.Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases[J].Nature,2006,443(7113):787-795.
[22] Li Y,Yang X,Ma C,et al.Necroptosis contributes to the NMDA-induced excitotoxicity in rat's cultured cortical neurons[J].Neurosci Lett,2008,447(2/3):120-123.
[23] Zhu S,Zhang Y,Bai G,et al.Necrostatin-1 ameliorates symptoms in R6/2 transgenic mouse model of Huntington's disease[J].Cell Death Dis,2011,2(1):e115.
[24] Pascual MJ,Reeds PJ.In vivo glucose contribution to glutamate synthesis is maintained while its contribution to acetyl CoA is lowered in adult mice fed a restricted amount of carbohydrate J[J].Nutr,1998,128(128):733-739.
[25] Liu J,Wu DC,Wang YT.Allosteric potentiation of glycine receptor chloride currents by glutamate[J].Nat Neurosci,2010,13(10):1225-1232.

备注/Memo

备注/Memo:
基金项目:国家科技部国际合作专项项目(编号2013DFA32610); 国家自然科学基金资助项目(81271450); 陕西省国际科技合作与交流计划项目(2015KW-035)
更新日期/Last Update: 2017-02-20