缺血性脑卒中白质损伤及保护的研究进展
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摘要
脑卒中严重危害人类的生命和健康,是成年人致残的主要原因,也是我国最常见的慢性病之一。脑卒中不仅严重损伤大脑灰质,还严重损伤白质。以往更加注重对大脑灰质的研究,而不够重视对白质损伤的作用,但在治疗上来看,就算灰质从损伤中恢复,而未对白质的损伤进行及时挽救,患者的治疗难以取得理想的效果。故应更加重视对白质损伤机制的深入理解,及时尽量恢复白质的功能。少突胶质细胞是脑白质的主要构成部分,对缺血性损伤极为敏感,保护少突胶质细胞免受缺血损伤及促进少突胶质细胞再生是维护缺血性卒中后白质完整性的重要手段。本文就白质损伤及保护的研究进展展开综述。
Stroke seriously endanger human life and health, is the main cause of disability in adults, but also one of the most common chronic diseases in our country. Stroke is not only serious damage to the brain gray matter, but also seriously damage the white matter. In the past, more attention was paid to the study of the gray matter of the brain, not to the importance of white matter damage. However, even if the gray matter is recovered from the injury and the white matter is not salvaged in time, the treatment of the patient is hard to achieve the desired effect. Therefore, more attention should be paid to the white matter damage mechanism in-depth understanding of the timely recovery of white matter function. Oligodendrocytes are a major component of white matter and are extremely sensitive to ischemic injury. Protecting oligodendrocytes from ischemic injury and promoting oligodendrocyte regeneration is essential for the maintenance of white matter integrity after ischemic stroke The important means. This article reviews the research progress of white matter damage and protection.
Stroke seriously endanger human life and health, is the main cause of disability in adults, but also one of the most common chronic diseases in our country. Stroke is not only serious damage to the brain gray matter, but also seriously damage the white matter. In the past, more attention was paid to the study of the gray matter of the brain, not to the importance of white matter damage. However, even if the gray matter is recovered from the injury and the white matter is not salvaged in time, the treatment of the patient is hard to achieve the desired effect. Therefore, more attention should be paid to the white matter damage mechanism in-depth understanding of the timely recovery of white matter function. Oligodendrocytes are a major component of white matter and are extremely sensitive to ischemic injury. Protecting oligodendrocytes from ischemic injury and promoting oligodendrocyte regeneration is essential for the maintenance of white matter integrity after ischemic stroke The important means. This article reviews the research progress of white matter damage and protection.
引文
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[2]Ovbiagele B,Nguyen-Huynh MN.Stroke epidemiology:advancing our understanding of disease mechanism andtherapy[J].Neuroth erapeutics,2011,8(3):319-329.
[3]Garbuzova-Davis S,Rodrigues MC,Hernandez-OntiverosDG.Bloodbrain barrier alterations provide evidence ofsubacute diaschisis in an ischemic stroke rat model[J].PLo S One,2013,8(5):e63553764-63553770.
[4]Ramesh G,Benge S,Pahar B,et al.A possible role for in-flammation in mediating apoptosis of oligodendrocytes asinduced by the Lyme disease spirochete Borrelia burgdor-fer[J].Neuroinflammation2012,9(1):72.
[5]Famakin BM.The immune response to acute focal cerebralischemia and associated post-stroke immunodepression:afocused review[J].Aging Dis,2014,5(5):307-326.
[6]Xiong X,White RE,Xu L,et al.Mitigation of murine focalcerebral isch-emia by the hypocretin/orexin system is as-sociated with reduced inflammation[J].Stroke,2013,44(3):764-770.
[7]Chen R,Xu M,Hogg RT,et al.The acetylase/deacetylasecouple CREB-binding rotein/Sirtuin 1 controls hypoxia-inducible factor 2 signaling[J].Biol Chem,2012,287(36):30800-30811.
[8]Baumann N,Pham-Dinh D.Biology of oligodendrocyte and myelin in themammalian central nervous system[J].Physiol Rev,2001,81(2):871-927.
[9]Zalc B,Goujet D,Colman D.The origin of the myelination program in vertebrates[J].Curr Biol,2008,18(12):8511-8512.
[10]Lee Y,Morrison BM,Li Y,et al.Oligodendroglia metabolically support axons and contribute to neurodegeneration[J].Nature2012,487(7408):443-448.
[11]Miller AK,Alston RL,Corsellis JA.Variation with age in the volumes of grey andwhite matter in the cerebral hemispheres of man:Measurements with an image analyser[J].Neuropathol Appl Neurobiol,1980,6(2):119-132.
[12]Gilles FH,Murphy SF.Perinatal telencephalic leucoencephalopathy[J].J Neurol Neurosurg Psychiatry,1969,32(5):404-413.
[13]Leviton A,Gilles FH.Acquired perinatal leukoencephalopathy[J]Ann Neurol,1984,16:1-8.
[14]McIver SR,Muccigrosso M,Gonzales ER,et al.Oligodendrocyte degeneration and recovery after focal cerebral ischemia[J].Neuroscience,2010,169(3):1364-1375.
[15]Nishizaki T,Yamauchi R,Tanimoto M,et al.Effects of temperature on theoxygen consumption in thin slices from different brain regions[J].Neurosci Lett,1988,86(3):301-305.
[16]Pantoni L,Garcia JH,Gutierrez JA.Cerebral white matter is highly vulnerable to ischemia[J].Stroke,1996,27(9):1641-1646.
[17]Filley CM.The behavioral neurology of cerebral white matter[J]Neurology,1998,50(6):1535-1540.
[18]Pantoni L,Leys D,Fazekas F,et al.Role of white matter lesions in cognitive impairment of vascular origin[J].Alzheimer Dis Assoc Disord,1999,13 Suppl 3:S49-S54.
[19]Desmond DW.Cognition and white matter lesions[J].Cerebrovasc Dis,2002,13 Suppl 2:53-57.
[20]Volpe JJ.Neurobiology of periventricular leukomalacia in the premature infant[J].Pediatr Res,2001,50(5):553-562.
[21]Goldberg MP,Ransom BR.New light on white matter[J].Stroke2003,34(2):330-332.
[22]Petito CK.Transformation of postischemic perineuronal glial cells.I.Electronmicroscopic studies[J].J Cereb Blood Flow Metab1986,6(5):616-624.
[23]Phillis JW,Goshgarian HG.Adenosine and neurotrauma:Therapeutic perspectives[J].Neurol Res,2001,23(2/3):183-189.
[24]Uchihara T,Tsuchiya K,Nakamura A,et al.Appearance of tau-2immunoreactivity in glial cells in human brain with cerebral infarction[J].Neurosci Lett,2000,286(2):99-102.
[25]Dewar D,Underhill SM,Goldberg MP.Oligodendrocytes and ischemic braininjury[J].J Cereb Blood Flow Metab,2003,23(3):263-274.
[26]Matute C,Alberdi E,Domercq M,et al.Excitotoxic damage to white matter[J].J Anat,2007,210(6):693-702.
[27]Stys PK.White matter injury mechanisms[J].Curr Mol Med,20044(2):113-130.
[28]Wender R,Brown AM,Fern Swanson RA,et al.Astrocyticglycogen influences axon function and survival during glucose deprivation in centralwhite matter[J].J Neurosci,2000,20(18):6804-6810.
[29]Alix JJ.The pathophysiology of ischemic injury to developing white matter.McGill J Med,2006,9(2):134-140.
[30]Monyer H,Burnashev N,Laurie DJ,et al.Developmental andregional expression in the rat brain and functional properties of four nmda receptors[J].Neuron,1994,12(3):529-540.
[31]Mc Tigue DM,Tripathi RB.The life,death,and replacement of oligodendrocytesin the adult cns[J].J Neurochemistry,2008,107(1):1-19.
[32]Gensert JM,Goldman JE.Endogenous progenitors remyelinate demyelinatedaxons in the adult cns[J].Neuron,1997,19(1):197-203.
[33]Franklin RJ.Why does remyelination fail in multiple sclerosis?[J]Nat Rev Neurosci,2002,3(9):705-714.
[34]Fancy SP,Chan JR,Baranzini SE,et al.Myelin regeneration:Arecapitulation of development?[J].Ann Rev Neurosci,2011,34:21-43.
[35]Alvarez-Buylla A,Kohwi M,Nguyen TM,et al.The heterogeneity of adultneural stem cells and the emerging complexity of their niche[J].Cold Spring Harb Quant Biol,2008,73:357-365.
[36]Menn B,Garcia-Verdugo JM,Yaschine C,et al.Origin of oligodendrocytes in the subventricular zone of the adult brain[J].JNeurosci,2006,26(30):7907-7918.
[37]Zhang RL,Chopp M,Roberts C,et al.Sildenafil enhancesneurogenesis and oligodendrogenesis in ischemic brain of middle-aged mouse[J].PIoS one,2012,7(10):e48141.
[38]Rafalski VA,Ho PP,Brett JO,et al.Expansion ofoligodendrocyte progenitor cells following sirtl inactivation in the adult brain[J]Nat Cell Biol,2013,15(6):614-624.
[39]Ortega F,Gascon S,Masserdotti G,et al.Oligodendrogliogenic and neurogenic adult subependymal zone neural stem cells constitute distinct lineages and exhibit differential responsiveness to wnt signalling[J].Nat Cell Biol,2013,15(6):602-613.
[40]Ueno Y,Chopp M,Zhang L,et al.Axonal outgrowthand dendritic plasticity in the cortical peri-infarct area after experimental stroke[J].Stroke,2012,43(8):2221-2228.
[41]Zhang RL,Chopp M,Roberts C,et al.Ascll lineage cells contribute to ischemia-induced neurogenesis and oligodendrogenesis[J].JCereb Blood Flow Metab,2011,31(2):614-625.
[42]Jablonska B,Aguirre A,Raymond M,et al.Chordin-induced lineage plasticity of adult svz neuroblasts after demyelination[J].Nat Neurosci,2010,13(5):541-550.
[43]Liu XS,Chopp M,Zhang XG,et al.Geneprofiles and electrophysiology of doublecortin-expressing cells in the subventricular zoneafter ischemic stroke[J].J Cereb Blood Flow Metab,2009,29(3):297-307
[44]Nait-Oumesmar B,Decker L,Lachapelle F,et al.Progenitor cells of the adult mouse subventricular zoneproliferate,migrate and differentiate into oligodendrocytes after demyelination[J].Eur JNeurosci,1999,11(12):4357-4366.
[45]De Castro F,Bribian A,Ortega MC.Regulation of oligodendrocyte precursor migration during development,in adulthood and in pathology[J].Cell Mol Life Sci,2013,70(22):4355-4368.
[46]Etxeberria A,Mangin JM,Aguirre A,et al.Adult-born svz progenitors receivetransient synapses during remyelination in corpus callosum[J].Nat Neurosci,2010,13(3):287-289.
[47]Dewar D,Underhill SM,Goldberg MP.Oligodendrocytes and ischemic brain injury[J].J Cerebral Blood Flow Metab,2003,23(3):263-274.
[48]Wakita H,Tomimoto H,Akiguchi I,et al.Axonal damage and demyelination in the white matter after chronic cerebral hypoperfusion in the rat.Brain Res,2002,924(1):63-70.
[49]Huber AB,Weimam O,Brosamle C,et al.Pattems of Nogo mRNAand protein expression in the developing and adult rat and after c Ns lesions[J].J Neurosci,2002,22(9):553-567.
[50]Buchli AD,Schwab ME.lnhibition of Nogo:a key strategy to increase regeneration,plasticity and functional recovery of the lesioned central nervous system[J].Ann Med,2005,37(8):556-567.
[51]Smailoglu UB,Saracoglu I,Harput US,et al.Effects of phenylpropanoid and iridoid glycosides on free radical-induded impairment of endothelium-dependent relaxation in rat aortic rings[J].JEthnopharmacol,2002,79(2):193-197.
[2]Ovbiagele B,Nguyen-Huynh MN.Stroke epidemiology:advancing our understanding of disease mechanism andtherapy[J].Neuroth erapeutics,2011,8(3):319-329.
[3]Garbuzova-Davis S,Rodrigues MC,Hernandez-OntiverosDG.Bloodbrain barrier alterations provide evidence ofsubacute diaschisis in an ischemic stroke rat model[J].PLo S One,2013,8(5):e63553764-63553770.
[4]Ramesh G,Benge S,Pahar B,et al.A possible role for in-flammation in mediating apoptosis of oligodendrocytes asinduced by the Lyme disease spirochete Borrelia burgdor-fer[J].Neuroinflammation2012,9(1):72.
[5]Famakin BM.The immune response to acute focal cerebralischemia and associated post-stroke immunodepression:afocused review[J].Aging Dis,2014,5(5):307-326.
[6]Xiong X,White RE,Xu L,et al.Mitigation of murine focalcerebral isch-emia by the hypocretin/orexin system is as-sociated with reduced inflammation[J].Stroke,2013,44(3):764-770.
[7]Chen R,Xu M,Hogg RT,et al.The acetylase/deacetylasecouple CREB-binding rotein/Sirtuin 1 controls hypoxia-inducible factor 2 signaling[J].Biol Chem,2012,287(36):30800-30811.
[8]Baumann N,Pham-Dinh D.Biology of oligodendrocyte and myelin in themammalian central nervous system[J].Physiol Rev,2001,81(2):871-927.
[9]Zalc B,Goujet D,Colman D.The origin of the myelination program in vertebrates[J].Curr Biol,2008,18(12):8511-8512.
[10]Lee Y,Morrison BM,Li Y,et al.Oligodendroglia metabolically support axons and contribute to neurodegeneration[J].Nature2012,487(7408):443-448.
[11]Miller AK,Alston RL,Corsellis JA.Variation with age in the volumes of grey andwhite matter in the cerebral hemispheres of man:Measurements with an image analyser[J].Neuropathol Appl Neurobiol,1980,6(2):119-132.
[12]Gilles FH,Murphy SF.Perinatal telencephalic leucoencephalopathy[J].J Neurol Neurosurg Psychiatry,1969,32(5):404-413.
[13]Leviton A,Gilles FH.Acquired perinatal leukoencephalopathy[J]Ann Neurol,1984,16:1-8.
[14]McIver SR,Muccigrosso M,Gonzales ER,et al.Oligodendrocyte degeneration and recovery after focal cerebral ischemia[J].Neuroscience,2010,169(3):1364-1375.
[15]Nishizaki T,Yamauchi R,Tanimoto M,et al.Effects of temperature on theoxygen consumption in thin slices from different brain regions[J].Neurosci Lett,1988,86(3):301-305.
[16]Pantoni L,Garcia JH,Gutierrez JA.Cerebral white matter is highly vulnerable to ischemia[J].Stroke,1996,27(9):1641-1646.
[17]Filley CM.The behavioral neurology of cerebral white matter[J]Neurology,1998,50(6):1535-1540.
[18]Pantoni L,Leys D,Fazekas F,et al.Role of white matter lesions in cognitive impairment of vascular origin[J].Alzheimer Dis Assoc Disord,1999,13 Suppl 3:S49-S54.
[19]Desmond DW.Cognition and white matter lesions[J].Cerebrovasc Dis,2002,13 Suppl 2:53-57.
[20]Volpe JJ.Neurobiology of periventricular leukomalacia in the premature infant[J].Pediatr Res,2001,50(5):553-562.
[21]Goldberg MP,Ransom BR.New light on white matter[J].Stroke2003,34(2):330-332.
[22]Petito CK.Transformation of postischemic perineuronal glial cells.I.Electronmicroscopic studies[J].J Cereb Blood Flow Metab1986,6(5):616-624.
[23]Phillis JW,Goshgarian HG.Adenosine and neurotrauma:Therapeutic perspectives[J].Neurol Res,2001,23(2/3):183-189.
[24]Uchihara T,Tsuchiya K,Nakamura A,et al.Appearance of tau-2immunoreactivity in glial cells in human brain with cerebral infarction[J].Neurosci Lett,2000,286(2):99-102.
[25]Dewar D,Underhill SM,Goldberg MP.Oligodendrocytes and ischemic braininjury[J].J Cereb Blood Flow Metab,2003,23(3):263-274.
[26]Matute C,Alberdi E,Domercq M,et al.Excitotoxic damage to white matter[J].J Anat,2007,210(6):693-702.
[27]Stys PK.White matter injury mechanisms[J].Curr Mol Med,20044(2):113-130.
[28]Wender R,Brown AM,Fern Swanson RA,et al.Astrocyticglycogen influences axon function and survival during glucose deprivation in centralwhite matter[J].J Neurosci,2000,20(18):6804-6810.
[29]Alix JJ.The pathophysiology of ischemic injury to developing white matter.McGill J Med,2006,9(2):134-140.
[30]Monyer H,Burnashev N,Laurie DJ,et al.Developmental andregional expression in the rat brain and functional properties of four nmda receptors[J].Neuron,1994,12(3):529-540.
[31]Mc Tigue DM,Tripathi RB.The life,death,and replacement of oligodendrocytesin the adult cns[J].J Neurochemistry,2008,107(1):1-19.
[32]Gensert JM,Goldman JE.Endogenous progenitors remyelinate demyelinatedaxons in the adult cns[J].Neuron,1997,19(1):197-203.
[33]Franklin RJ.Why does remyelination fail in multiple sclerosis?[J]Nat Rev Neurosci,2002,3(9):705-714.
[34]Fancy SP,Chan JR,Baranzini SE,et al.Myelin regeneration:Arecapitulation of development?[J].Ann Rev Neurosci,2011,34:21-43.
[35]Alvarez-Buylla A,Kohwi M,Nguyen TM,et al.The heterogeneity of adultneural stem cells and the emerging complexity of their niche[J].Cold Spring Harb Quant Biol,2008,73:357-365.
[36]Menn B,Garcia-Verdugo JM,Yaschine C,et al.Origin of oligodendrocytes in the subventricular zone of the adult brain[J].JNeurosci,2006,26(30):7907-7918.
[37]Zhang RL,Chopp M,Roberts C,et al.Sildenafil enhancesneurogenesis and oligodendrogenesis in ischemic brain of middle-aged mouse[J].PIoS one,2012,7(10):e48141.
[38]Rafalski VA,Ho PP,Brett JO,et al.Expansion ofoligodendrocyte progenitor cells following sirtl inactivation in the adult brain[J]Nat Cell Biol,2013,15(6):614-624.
[39]Ortega F,Gascon S,Masserdotti G,et al.Oligodendrogliogenic and neurogenic adult subependymal zone neural stem cells constitute distinct lineages and exhibit differential responsiveness to wnt signalling[J].Nat Cell Biol,2013,15(6):602-613.
[40]Ueno Y,Chopp M,Zhang L,et al.Axonal outgrowthand dendritic plasticity in the cortical peri-infarct area after experimental stroke[J].Stroke,2012,43(8):2221-2228.
[41]Zhang RL,Chopp M,Roberts C,et al.Ascll lineage cells contribute to ischemia-induced neurogenesis and oligodendrogenesis[J].JCereb Blood Flow Metab,2011,31(2):614-625.
[42]Jablonska B,Aguirre A,Raymond M,et al.Chordin-induced lineage plasticity of adult svz neuroblasts after demyelination[J].Nat Neurosci,2010,13(5):541-550.
[43]Liu XS,Chopp M,Zhang XG,et al.Geneprofiles and electrophysiology of doublecortin-expressing cells in the subventricular zoneafter ischemic stroke[J].J Cereb Blood Flow Metab,2009,29(3):297-307
[44]Nait-Oumesmar B,Decker L,Lachapelle F,et al.Progenitor cells of the adult mouse subventricular zoneproliferate,migrate and differentiate into oligodendrocytes after demyelination[J].Eur JNeurosci,1999,11(12):4357-4366.
[45]De Castro F,Bribian A,Ortega MC.Regulation of oligodendrocyte precursor migration during development,in adulthood and in pathology[J].Cell Mol Life Sci,2013,70(22):4355-4368.
[46]Etxeberria A,Mangin JM,Aguirre A,et al.Adult-born svz progenitors receivetransient synapses during remyelination in corpus callosum[J].Nat Neurosci,2010,13(3):287-289.
[47]Dewar D,Underhill SM,Goldberg MP.Oligodendrocytes and ischemic brain injury[J].J Cerebral Blood Flow Metab,2003,23(3):263-274.
[48]Wakita H,Tomimoto H,Akiguchi I,et al.Axonal damage and demyelination in the white matter after chronic cerebral hypoperfusion in the rat.Brain Res,2002,924(1):63-70.
[49]Huber AB,Weimam O,Brosamle C,et al.Pattems of Nogo mRNAand protein expression in the developing and adult rat and after c Ns lesions[J].J Neurosci,2002,22(9):553-567.
[50]Buchli AD,Schwab ME.lnhibition of Nogo:a key strategy to increase regeneration,plasticity and functional recovery of the lesioned central nervous system[J].Ann Med,2005,37(8):556-567.
[51]Smailoglu UB,Saracoglu I,Harput US,et al.Effects of phenylpropanoid and iridoid glycosides on free radical-induded impairment of endothelium-dependent relaxation in rat aortic rings[J].JEthnopharmacol,2002,79(2):193-197.