急性CO中毒后迟发性脑病大鼠模型中脑损伤与免疫炎症因子表达的研究
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
一氧化碳(carbon monoxide,CO)中毒是当今发生率和死亡率最高的中毒。它见于火灾,机动车尾气异常泄漏和工业或家庭燃气炉取暖、做饭及沐浴等发生的事故中,也有用CO自杀者。在CO中毒者中,3%~30%的患者中毒后经过一段时间的“假愈期”(数日或数周),又出现以痴呆、精神症状和锥体外系症状为主的神经系统疾病,称为CO中毒后迟发性脑病(delayed neuropsychologic sequelae,DNS),目前其发病机制仍未阐明。
     免疫系统的基本生理功能是对抗原物质进行免疫应答,通过免疫细胞引起的免疫炎症反应达到清除抗原物质的效应。近年来关于中枢免疫特点的研究表明中枢神经系统(central nervous system,CNS)并不是传统所认为的“免疫特免区”,在特定条件下,CNS的血脑屏障通透性会发生改变,允许血液中的免疫成分进入脑中,同时CNS存在着自己的抗原呈递细胞和免疫效应细胞,能释放各种免疫活性因子和发挥吞噬抗原的作用。CO中毒患者脑中急性期病理改变涉及兴奋性氨基酸毒性作用和氧化应激损伤等因素,脑组织在这些因素的作用下,极有可能发生蛋白变性等
Carbon monoxide (CO) poisoning is a venenation with high incidence rate and mortality rate. It can be seen in the situation of fire disaster, excessive revelation of motors' end gas, and accidents happened in industry or in the use of stove for heating, cooling and bathing in our daily life. Suicide with CO also can be heard sometime. In the patients of CO poisoning, 3%-30% will develop the delayed neuropsychologic sequelae (DNS ) which is characterized by dementia, psychiatric symptoms and extrapyramidal symptoms after a period of latent phase (days to weeks). Yet , the pathogenesis of DNS has not been elucidated.
    The basic function of immune system is to react to the substance of antigen. With the immunological inflammation reaction activated by the immunocell, body can clean up the substance of antigen. Recently , a lot of reports about the character of central nervous system (CNS) have shown that
引文
[1] Meyers RAM, Thom SR. Carbon monoxide and cyanide poisoning [A]. In: Kindwall EP, ed. Hyperbaric Medicine practice. Best Publishing Company, 1995; 343-372.
    [2] Piantadosi CA. Carbon monoxide poisoning [J]. Undersea Hyperb Med, 2004; 31: 167-177.
    [3] Ishiropoulos H, Beers MF, Ohnishi ST, et al. Nitric oxide production and perivascular nitration in urain after carbon monoxide in the rat. J Clin Invest, 1996; 97(10): 2260-2267.
    [4] Piantadosi CA, Zhang J, Demchenco IT. Production of hydroxl radical in the hippocampus after CO hypoxia or hypoxic hypoxia in the rats. Free Radic Biol Med, 1997; 22: 725-32.
    [5] Kreutzberg GW. Microglia: a sensor for pathological events in the CNS. Trends Neurosci, 1996; 19: 312-318.
    [6] Thom SR, Bhopale VM, Fisher D, et al. Delayed neuropathology after carbon monoxide poisoning is innune-mediated [J]. Proceedings National Academy of Science, 2004; 01: 13660-13665.
    [7] Fabry Z, Walschmidt MM, Hendrickson D, et al. Adhesion molecules on murine brain microvascular endothelial cells: expression and regulation of ICAM-1 and Lgp55. J Neuro immunol, 1992; 36:1.
    [8] 李海霞.急性一氧化碳中毒神经系统后发症15例分析.中西医结合心脑血管病杂志,2005;3(7):647-648.
    [9] 孟宪辉,耿月华,王怀敏.急性一氧化碳中毒后迟发性脑病40例报告.实用神经疾病杂志,2004;7(5):52-53.
    [10] 余海,潘晓雯,孟娟等.一氧化碳中毒迟发性脑病的临床研究.中华劳动卫生职业病杂志,2002;20(1):26-28.[11] 房广才.主编.一氧化碳中毒[M].北京:军事医学科学出版社,2001.126.
    [12] 贾和平,郑荣珍,崔现.急性CO中毒后迟发性脑病的相关因素及P300的研究[J].临床神经病学杂志,2002;15(3):277.
    [13] Murata T, Kimura H, Kado H, et al. Neuronal damage in the interval form of CO poisoning determined by serial diffusion weighted magnetic resonance imaging plus 1 H-magnetic resonance spectroscopy. J Neurol Neurosurg Psychiatry, 2001; 71(2): 250
    [14] 徐辰,于绍斌,薛宏斌,等.CO中毒后迟发性脑病的临床与脑电图、脑CT分析[J].现代电生理学杂志,2003;10(4):1852187.
    [15] 丁伟利,张向芬,刘春云.重度一氧化碳中毒并迟发脑病的高危因素分析.临床荟萃,2005;15(6):257.
    [16] 崔宏经.急性一氧化碳中毒神经系统并发症的防治体会.职业医学,1989;16(1):59.
    [17] 苏会涛,宋或林,王一兵.急性一氧化碳中毒及迟发脑病180例治疗体会.中国冶金工业医学杂志,2003;20(2):98.
    [18] Scheinkestel CD, Bailey M, Myles PS, et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial. Med J Aust, 1999, 170(5): 203-210.
    [19] 王国强,孟庆莲.一氧化碳中毒后脑梗塞[J].脑与神经疾病杂志,2000;1(8):60。
    [20] 翟峰,刘树娟,刘存学.1,6—二磷酸果糖治疗急性CO中毒后迟发性脑病临床观察[J].医学理论与实践,2003;16(11):1270-1271.
    [21] Wada K, Miyazawa T, Nomura N, et al. Mn-SOD and Bcl-2 expression after repeated hyperbaric oxygenation [J]. Acta Neurochir Suppl, 2000; 76: 285-90.[22] Piantadosi CA, Zhang J, Levin ED, et al. Apoptosis and delayed neuronal damage after carbon monoxide poisoning in the rat [J]. Exp Neurol, 2000; 147(1): 103-14.
    [23] Piantadosi CA, Zhang J, Levin ED, et al. Apoptosis and delayed neuronal damage after carbon monoxide poisoning in the rat [J]. Exp Neural, 1997; 147(1)103-114.
    [24] 刘颖菊,杨梭卿,周歧新,等.急性一氧化碳中毒致脑细胞凋亡及相关基因表达 [J].工业卫生与职业病,2000;26(5):257-260.
    [25] 陈春富,刘凤超,郭述苏,等.一氧化碳中迟发性脑病大鼠模型复制方法 [J].中国病理生理杂志,2004;20(2):286-288.
    [26] 刘凤超,郭述苏,吕保生.一氧化碳中毒所致迟发性脑病大鼠模型的建立 [J].中华医学杂志,2002;82(23):1645-1648.
    [27] Piantadosi CA, Zhang J, Demchenco IT. Production of hydroxl radical in the hippocampus after CO hypoxia or hypoxic hypoxia in the rats. Free Radical Biol Med. 1997; 22: 725-32.
    [28] Newman TA, Wooley ST, Hughes PM, et al. T-cell-and-macrophage-mediated axon damage in the absence of a CNS-specific immune response: inovement of metalloproteinases. Brain, 2001; 24: 2203-2214.
    [29] Thom SR, Fisher D, Xu YA, et al. Role of nitric oxide-derived oxidants in vascular injury from carbon monoxide in the rat [J]. Am. J. Physiol, 1999; 276 (3): H984-H992.
    [30] Bradt DS, Snyder SH. Nitric oxide, a novel neuronal messenger [J]. Neuron, 1992; 8: 3~11.
    [31] Maines MD. The heme oxygenase system: a regulator of second messenger gases. Annu Rev Pharmacol Toxicol, 1997; 37: 517-554.[32] 温韬,赵金垣,赵伯阳.一氧化碳中毒迟发脑病与内源性一氧化碳.中华劳动卫生职业杂志,2002;20(1):72
    [33] 刘青乐,蔡溱,金智锋.一氧化碳暴露对Wistar大鼠脑中p53基因表达的影响.中华航海医学与高气压医学杂志,2002;9(3):141.
    [34] 张秀明,简国庆,高耀东.急性CO中事后迟发性脑病患者脑脊液髓鞘碱性蛋白和三种酶测定的意义[J].上海医学检验杂志,2003;18(3):142-144
    [35] Bergman H, Nagy JI, Granholm AC. Intracranial transplantation and survival of tuberomammillary histaminergic neurons. Neuroscience, 1995; 64(1): 61-70.
    [36] Poser CM. Notes on the pathogenesis of multiple sclerosis. Clin Neurosci, 1994; 2: 258-265.
    [37] Gay D, Esiri M. Blood-brain barrier damage in acute multiple sclerosis plaques: an immunocytological study. Brain, 1991; 114: 557-572.
    [38] Proescholdt MA, Heiss JD, Walbridge S, et al. Vascular endothelial growth factor (VEGF) modulates vascular permeability and inflammation in rat brain. J Neuropathol Exp Neurol, 1999; 58: 613-627.
    [39] 武士京,陈世唆.血脑屏障—免疫学研究新进展.现代神经疾病杂志,2003;3(5):311-314.
    [40] 邝芳.血脑屏障与免疫介质[J].国外医学神经病学神经外科学分册,2000;27(3):156-159.
    [41] Aloisi F, Ria F, Adorini L. Regulation of T-cell responses by CNS antigenpresenting cells: different roles for microglia and astrocytes[J]. Immunol Today, 2000; 21 (3): 141-147.
    [42] Becher B, Prat A, Antel JE Brain-immune connection: immuno-regulatory properties of CNS-resident cells. Glia, 2000 Feb 15; 29(4):??293-304.
    
    [43] Horwitz MS, Evans CF, Klier FG, et al . Detailed in vivo analysis of interferon - gamma induced major histocompatibility complex expression in the central nervous system: astrocytes fail to express major histocompatibility complex class I and II molecules [J]. L ab Invest, 1999; 79 (2):235 -242.
    
    [44] De Simone R, Giampaolo A, Giometto B, et al. The costimulatory molecule B7 is expressed on human microglia in culture and in multiple sclerosis acute lesions [J]. J Neuropathol Ex p Neurol, 1995; 54 (2): 175-187.
    
    [45] Shrikant P, Benveniste EN. The central nervous system as an immunocompetent organ: role of glial cells in antigen presentation [J]. J Immunol, 1996; 157(5): 1819-1822.
    
    [46] Aloisi F, De Simone R, Columba-Cabezas S, et al. Functional maturation of adult mouse resting microglia into an APC is promoted by granulocyte - macrophage colony - stimulating factor and interaction with Th1 cells [J]. J Immunol, 2000; 164(4): 1705-1712.
    
    [47] Matyszak MK. Inflammation in the CNS: balance between immunological privilege and immune responses [J]. Prog Neurobiol, 1998; 56 (1):19-35.
    
    [48] Aloisi F, Ria F, Columba - Cabezas S, et al. Relative efficiency of microglia , astrocytes , dendritic cells and B cells in naive CD4 + T cell priming and Th1/ Th2 cell restimulation [J]. Eur J Immunol, 1999; 29 (9):2705-2714.
    
    [49] Carson MJ, Reilly CR, Sutcliffe J G, et al. Mature microglia resemble immature antigen - presenting cells [J]. Glia, 1998; 22(1):72-85.
    
    [50] Aloisi F. Immunefunction of microglia [J]. Glia, 2001; 36(2): 165-179.
    
    [51] Hanisch UK. Microglia as a source and target of cytokines [J]. Glia, 2002;40(2):140-155.
    
    [52] Colton AC, Gilbert DL. Production of superoxide anions by a CNS macrophage, the microglia. FEBS Lett, 1987; 223:284-288.
    
    [53] Love S. Oxidative stress in brain ischemia. Brain Pathol, 1999; 9:119-131.
    
    [54] Merrill JE, Ignarro LJ, Sherman MP, et al. Microglial cell cytotoxicity of oligodendrocytes in mediated through nitric oxide. J Immunol, 1993; 151: 2132-2141.
    
    [55] Acarin L, Gonzalez B, Castellano B, et al. Microglial response to N-methyl-D-aspartate-mediated excitotoxicity in the immature rat brain. J Comp Neurol, 1996; 367:361-374.
    
    [56] Sairanen TR, Lindsberg PJ, Brenner M, et al. Global forebrain ischemia results in differential cellular expression of interleukin-1β (IL-1β) and its receptor at mRNA and protein level. J Cereb Blood Flow Metab, 1997; 17:1107-1120.
    
    [57] Chao CC, Hu S. Tumour necrosis factor-a potentiates glutamate neurotoxicity in human fetal brain cell cultures. Dev Neurosci, 1994; 16:172-179.
    
    [58] Merrill JE, Zimmerman RP. Natural and induced cytotoxicity of oligodendrocytes by microglia is inhibitable by TGF-β. Glia, 1991; 4:327-331.
    
    [59] Hoftberger R, Aboul-Enein F, Brueck W, et al. Expression of major histocompatibility complex class I molecules on the different cell types in multiple sclerosis lesions. Brain Pathol, 2004; 14(1):43-50.
    
    [60] Lerner-Natoli M, Montpied P, Rousset MC, et al. Sequential expression of surface antigens and transcription factor NFkappaB by hippocampal cells in excitotoxicity and experimental epilepsy. Epilepsy Res, 2000; 41 (2): 141-154.
    
    [61] Nitta T, Yagita H, Sato K, et al. Expression of Fc gamma receptors onastroglial cell lines and their role in the central nervous system. Tem. Neurosurgery, 1992; 31(1): 83-88.
    [62] Candore G, Balistreri CR, Colonna-Romano G, et al. Major histocompatibility complex and sporadic Alzheimer's disease: a critical reappraisal. Exp Gerontol, 2004; 39: 645-652.
    [63] 高晶,郭玉璞.缺血后脑组织损伤中的炎细胞作用.中华神经科杂志,1999:32:303-305.
    [64] 黄诚,陈汉平,程介士.白细胞介素1和缺血性脑损伤[J].生理科学进展,1997;28(2):175-177.
    [65] Loddick SA, Wong ML, Bongiorno PB, et al. Endogenous interleukin-1 receptor antagonist is neuroprotective. Biochem Biophys Res Commun, 1997; 234: 211-215.
    [66] Stroemer RP, Rothwell NJ. Exacerbation of ischemic brain damage by localized striatal injection of intedeukin-1 beta in the rat. J Cereb Blood Flow Metab, 1998; 18: 833-839.
    [67] Stroemer RP, Rothwell NJ. Cortical protection by localized striatal injection of IL-1rα following cerebral ischemia in the rat. J Cereb Blood Flow Metab, 1997; 17: 597-604.
    [68] Min SK. A brain syndrome associated with delayed neuropsychiatric sequelae following acute carbon monoxide intoxication [J]. Acta Psychiatrica Stand, 1986; 73: 80-85.
    [69] 胡镜清,温泽淮,赖世隆.Morris水迷宫检测的记忆属性与方法学初探 [J].广州中医药大学学报,2004;17(2):117-119.
    [70] Grant MJC, Clay B. Accidental Carbon Monoxide Poisoning With Severe Cardiorespiratory Compromise in 2 Children [J]. Am. J. Crit. Care, 2002; 11: 128-131.[71] Powers WE. Delayed presentation of carbon monoxide poisoning. J Emerg Med, 1999; 17(5): 905-906
    [72] Nabeshima T, Katoh K, Ishimaru H, et al. Carbon monoxide induced delayed amnesia, delayed neuronal death and change in acetylcholine concentrationinmice [J]. J Pharmacol Exp Ther, 1991; 256(2): 378-383.
    [73] 张镭.一氧化碳中毒后迟发性脑病的CT特性[J].临床医学影像杂志,1998:9:93-96.
    [74] Inagaki T, Ishino H, Seno H, et al. A long-term follow-up study of serial magnetic resonance images in patients with delayed encephalopathy after acute carbon monoxide poisoning [J]. Psychiatry Clin Neurosci, 1997; 51(6): 421-423.