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The role of microglia cells in cerebral ischemia reperfusion injury |
QI Ya′nan1,2 GUO Dazhi2 PAN Shuyi1,2 |
1.Gracluate School, Chengde Medical College, Hebei Province, Chengde 067000, China;
2.Department of Hyperbaric, the Sixth Medical Center of Chinese PLA General Hospital, Beijing 100089, China |
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Abstract Neuroinflammatory reaction plays an important role in the pathophysiology of cerebral ischemia-reperfusion injury. Microglia is an important immune effector cell in the central nervous system (CNS), and it is the first defensive line for CNS. Microglia can release a variety of inflammatory factors and a variety of growth factors and increase the expression of various proinflammatory enzymes. It plays a key role in the neuroinflammatory reactions. During cerebral ischemia-reperfusion injury occurs, microglia cells are activated by a variety of cytokines at“rest”, such as γ-interferon, tumor cytokine-α, colony stimulating factor, transforming growth factor, etc. Then it transforms into different phenotypes of “activated” microglia, namely M1 and M2 type. They play a dual effect of anti-inflammatory and pro-inflammatory, and affect the occurrence and development of cerebral ischemia-reperfusion injury. This review describes the physiological characteristics of microglia, factors affecting microglia activation, phenotypic transformation characteristics of microglia and factors regulating phenotypic changes, in order to understand the role of microglia in cerebral ischemia reperfusion injury, and characteristics of activation and phenotypic transformation. It provides the basis for the prevention, treatment and prognosis of cerebral ischemia-reperfusion injury.
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[1] 陈礼刚,江涌.重新认识创伤性脑损伤后的神经炎症反应[J].中华神经外科疾病研究杂志,2017,16(4):289-292.
[2] Mizuma A,Yenari MA. Anti-Inflammatory Targets for the Treatment of Reperfusion Injury in Stroke. [J]. Front Neurol,2017,8:467.
[3] 张琼,刘文娟,曹霞.小胶质细胞特性及其功能的研究进展[J].医学研究生学报,2017,30(2):216-219.
[4] Cherry JD,Olschowka JA,Obanion MK. Neuroinflammation and M2 microglia:the good,the bad,and the inflamed [J]. J Neuroinflammation,2014,11:98.
[5] Prinz M,Priller J. Microglia and brain macrophages in the molecular age:from origin to neuropsychiatric disease [J]. Nat Rev Neurosci,2014,15(5):300-312.
[6] Eyo UB,Dailey ME. Microglia:Key Elements in Neural Development,Plasticity,and Pathology [J]. J Neuroimmune Pharmacol,2013,8(3):494-509.
[7] David S,Kroner A. Repertoire of microglial and macrophage responses after spinal cord injury [J]. Nat Rev Neurosci,2011,12(7):388-399.
[8] Parkhurst CN,Yang G,Ninan I,et al. Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor [J]. Cell,2013,155(7):1596-1609.
[9] 向彬,申婷,肖纯,等.小胶质细胞在缺血性脑卒中后活化特点的研究进展[J].中国医药导报,2017,14(9):31-33.
[10] 杜一星,王伟.小胶质细胞的活化与调控[J].国际脑血管病杂志,2004,12(8):624-626.
[11] 张梅,田英,刘翠平.肿瘤坏死因子与脑卒中的炎症反应关系研究进展[J].现代中西医结合杂志,2011,20(16):2079-2080.
[12] Gehrmann J,Matsumoto Y,Kreutzberg GW. Microglia:intrinsic immuneffector cell of the brain [J]. Brain Res Rev,1995,20(3):269-287.
[13] Pang L,Ye W,Che XM,et al. Reduction of inflammatory response in the mouse brain with adenoviral-mediated transforming growth factor-ss1 expression [J]. Stroke,2001, 32(2):544-552.
[14] Miron VE,Boyd A,Zhao JW,et al. M2 microglia and mac-rophages drive oligodendrocyte differentiation during CNS remyelination [J]. Nat Neurosci,2013,16(9):1211-1218.
[15] 赵晶晶.钾离子通道亚型Kv1.3参与甲基苯丙胺引起小胶质细胞的损伤[D].江苏:南京医科大学,2013.
[16] Mu?觡ozplanillo R,Kuffa P,Martínezcolón G,et al. K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter [J]. Immunity,2013,38(6):1142-1153.
[17] 高艳.小胶质细胞生理特点及在脑缺血损伤中的作用[J].中国组织化学与细胞化学杂志,2012,21(6):598-602.
[18] Surinkaew P,Sawaddiruk P,Apaijai N,et al. Role of microglia under cardiac and cerebral is chemia/reperfusion(I/R)injury [J]. Metab Brain Dis,2018,33(4):1019-1030.
[19] Luo XL,Liu SY,Wang LJ,et al. A tetramethoxychalcone from Chloranthus henryi suppresses lipopolysaccharide-induced inflammatory responses in BV2 microglia [J]. Eur J Pharmacol,2016,774:135-143.
[20] Sieweke MH,Allen JE. Beyond Stem Cells:Self-Renewal of Differentiated Macrophages [J]. Science,2013,342(6161):1242974.
[21] 杨俭,冉媛媛,张妍,等.传统观念的转变:极化的小胶质细胞/巨噬细胞在中枢神经系统修复中的双重作用[J].生命科学仪器,2015,13(6):5-10.
[22] Lisi L,Stigliano E,Lauriola L,et al. Proinflammatory-activated glioma cells induce a switch in microglial polarization and activation status,from a predominant M2b phenotype to a mixture of M1 and M2a/B polarized cells [J]. ASN Neuro,2014,6(3):171-183.
[23] Patel AR,Ritzel R,Mc Cullough LD,et al. Microglia and ischemic stroke:a double-edged sword [J]. Int J Physiol Pathophysiol Pharmacol,2013,5(2):73-90.
[24] Miron VE,Boyd A,Zhao JW,et al. M2 microglia and mac-rophages drive oligodendrocyte differentiation during CNS remyelination [J]. Nat Neurosci,2013,16(9):1211-1218.
[25] 耿悦,田雪松.缺血性脑损伤状态下小胶质细胞的极化现象与影响因素[J].神经解剖学杂志,2017,33(4):503-507.
[26] 杜可,潘彦竹,钟欣,等.内质网应激与巨噬细胞M1/M2极化的研究进展[J].解剖科学进展,2017(2):91-93,97.
[27] 马绥斌,曹成慧,刘霞,等.小胶质细胞极化态的功能可塑性调控[J].生命的化学,2017,37(5):859-866.
[28] Orihuela R,Mcpherson CA,Harry GJ. Microglial M1/M2 polarization and metabolic states [J]. Br J Pharmacol,2015,173(4):649-665.
[29] Ferrante CJ,Pinhal-Enfield G,Elson G,et al. The adenosine-dependent angiogenic switch of macrophages to an M2-like phenotype is independent of interleukin-4 receptor alpha (IL-4Ralpha) signaling [J]. Inflammation,2013,36(4):921-931.
[30] 王栋,侯博儒,杨文桢,等.缺血性脑卒中后小胶质细胞损伤作用的研究进展[J].中国康复理论与实践,2017, 23(1):42-45.
[31] Xu Y,Qian L,Zong G,et al. Class A scavenger receptor promotes cerebral ischemic injury by pivoting microglia/macrophage polarization [J]. Neuroscience,2012,218:35-48.
[32] Pérez-De PI,Miró F,Salas-Perdomo A,et al. IL-10 deficiency exacerbates the brain inflammatory response to permanent ischemia without preventing resolution of the lesion [J]. J Cereb Blood Flow Metab,2013,33(12):1955-1966.
[33] Liu X,Liu J,Zhao S,et al. Interleukin-4 is Essential for Microglia/Macrophage M2 Polarization and Long-term Recovery after Cerebral Ischemia [J]. Stroke,2016,47(2):498-504. |
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