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补体激活在中枢神经系统损伤中的作用 被引量:2

Complement activation in central nervous system injury
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摘要 补体系统是机体固有免疫系统的重要组成部分,中枢神经系统的神经元、星形胶质细胞及小胶质细胞可以产生几乎所有的补体系统组分,表达各种补体受体。神经科学研究发现,补体系统在中枢神经系统正常功能及一些疾病中都有重要的作用。补体广泛参与神经系统的发育、突触消除、神经网络的成熟等生理过程。在各种中枢神经系统损伤中,包括脑或脊髓外伤性损伤、脑或脊髓缺血再灌注损伤,补体也参与其病理进程。很多研究表明在发生神经系统损伤时,抑制补体激活具有神经保护作用,这也为预防和治疗中枢神经系统损伤提供了新的思路。 The complement system is a major component of the innate immune system. Several studies have dem- onstrated that virtually all of the components of complement can be synthesized within the CNS and a variety of comple- ment receptors were expressed on neurons, astrocytes and mieroglial cells. Complement activation participated in various aspects of both normal central nervous system (CNS) function and pathology. Various studies have revealed particularly novel findings on the wide-ranging involvement of complement in neural development, synapse elimination and maturation of neural networks. In addition, the progression of pathology in a range of brain or spinal cord injury, including ischemia- reperfusion injury or stroke, traumatic brain injury (TBI) and spinal cord injury (SCI), where rapid disruption of neuro- nal homeostasis potently triggers complement activation. Inhibition of complement activation had been found neuroprotec- tire effects in the CNS injury. So complement-targeted therapeutics maybe a new method to alleviate the devastating con- sequences of these neurological conditions.
作者 董全 巩守平
出处 《西部医学》 2013年第12期1906-1908,共3页 Medical Journal of West China
基金 国家自然科学基金资助项目(30973023)
关键词 补体激活 中枢神经系统 损伤 Complement activation Central nervous system Injury
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参考文献32

  • 1Rieklln D, Hajishengallls G, Yang K. Lambris JD: Comple- ment., a key system for immune surveillance and homeostasis[J]. Nat Immunol, 2010, 11:785-797. 被引量:1
  • 2Wagner E. Frank MM: Therapeutic potential of complement modulation[J]. Nat Rev Drug Discov, 2010, 9:43-56. 被引量:1
  • 3Gasque P, Dean YD, McGreal EP, etal. Morgan BP: Comple- ment components of the innate immune system in health and dis- ease in the CNS[J]. Immunopharmacology, 2000, 49:171-186. 被引量:1
  • 4Galvan MD, Luchetti S, Burgos AM, Nguyen HX, Hooshmand MJ, Hamers FPT, Anderson AJ : Deficiency in complement Clq improves histological and functional locomotor outcome after spi- nal cord injury[J]. J Neurosci, 2008, 28:13876-13888. 被引量:1
  • 5Arumugam TV, Woodruff TM, Lathia JD, et al. Taylor SM: Neuroprotection in stroke by complement inhibition and immu- noglobulin therapy[J]. Neuroscience, 2009, 158:1074-I089. 被引量:1
  • 6杨玺,史忠.颅脑创伤的药物治疗进展[J].西部医学,2007,19(6):1182-1185. 被引量:6
  • 7Moeeo J, Wilson DA, Komotar RJ, et al. Connolly ES Jr: Al- terations in plasma complement levels alter human ischemie stroke[J]. Neurosurgery, Z006, 59:28-33. 被引量:1
  • 8Pedersen ED, Loberg EM, Vege E, et al. Mollnes TE: In situ deposition of complement in human acute brain ischaemia[J]. Seand J Immunol, 2009, 69:555-562. 被引量:1
  • 9Cervera A, Planas AM, Justicia C, etal. Chamorro A: Geneti- cally-defined deficiency of mannose-binding lectin is associated with protection after experimental stroke in mice and outcome in human stroke[J]. PLoS One, 2010, 5;e8433. 被引量:1
  • 10Gesuete R, Storinl C, Fantin A, etal. De Simoni MG; Recom- binant C1 inhibitor in brain ischemic injury[J]. Ann Neurol, 2009, 66:332-342. 被引量:1

二级参考文献21

  • 1Chiang J,Kowada M, Ames A,et al. Cerebral ischemia III Vas- cular changes[J]. Am J Pathol,1968, 52(2) :455-476. 被引量:1
  • 2McCord JM. Oxygen-derived free radicals in postischemic tissueinjury[J]. New Eng J Med,1985, 312(3):159-163. 被引量:1
  • 3Li S, Stys PK. Mechanisms of Ionotropic Glutamate Receptor Mediated Excitot oxicity in Isolated Spinal Cord White Matter [J]. The Journal of Neuroscience,2000,20(3) : 1190-1198. 被引量:1
  • 4Basu S, Hellberg A, Ulus AT, et al. Biomarkers of free radical injury during spinal cord ischemia[J].FEBS Letters, 2001,508 (1) ,36-38. 被引量:1
  • 5Peasley MA, Shi R. Ischemie insult exacerbates acrolein-indueed conduction Loss and axonal membrane disruption in guinea pig spinal cord white matter[J]. J Neurol Sci, 2003, 216(1) :23-32. 被引量:1
  • 6Emerich DF, Dean RL 3rd, Bartus RT. The Role of Leukocytes Following Cerebral Ischemia: Pathog-enic Variable or Bystander Reaction to Emerging Infarct[J]. Experimental Neurology, 2002, 173:168-181. 被引量:1
  • 7Maureen McMichael. Ischemia-reperfusion injury: assessment and treatment, part II [J]. Journal of Veterinary Emergency and Critical Care,2004,14(4) .. 242-252. 被引量:1
  • 8Michael P, Murphy. Nitric oxide and cell death [J]. Biochimica and Biophysica Acta, 1999, 1411(2-3) : 401-414. 被引量:1
  • 9Sakurai M, Hayashi T, Abe K,et a l. Delayed and selective motor neuron death after transient spinal cord isehemiat a role of apop- tosis[J]. J of Thoracic & Cardiovascular Surgery, 1998, 115 (6) : 1310-1315. 被引量:1
  • 10Kiyoshima T, Fukuda S, Matsumoto M, et al. Lack of evidence for apoptosis as a cause of delayed onset paraplegia after spinal cord ischemia in rabbits [J]. International Anesthesia Research Society, 2003,96(3) :839-846. 被引量:1

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