缺血后脑组织损伤中的炎细胞作用
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资料包括： 论文(5页4898字)
说明：
关键词： 脑,缺血损伤,促炎性细胞因子
脑动脉阻断后即使立即再通，脑组织的缺血损伤也不能完全恢复正常，而且不能完全挽救由继发损伤造成的脑缺血组织的继续扩大［1］。缺血后脑死亡的机制可能与组织酸中毒、神经元释放兴奋性氨基酸、细胞内钙聚集、氧化应激（蛋白氧化、脂质过氧化、DNA氧化）、一氧化氮合成、微循环损害及弥散性去极化抑制等有关。目前，较多的研究兴趣集中在缺血再灌注后的炎性过程，缺血细胞以及缺血激活的内皮细胞、白细胞，产生促炎性细胞因子，表达粘附分子，导致白细胞积聚和外流［1］。有些作者认为，缺血后导致细胞死亡的主要因素之一可能是白细胞浸润，甚至提出脑缺血治疗的途径一是再通动脉，二是抑制细胞因子的促炎性作用［2］。现将有关的研究报道综述如下。
一、脑缺血后炎性细胞的变化
1.动物实验的依据：缺血脑组织可检到CD11和CD18阳性浸入的白细胞；OX42免疫反应的向上调节可显示伴形态变化的激活小胶质细胞以及在激活的小胶质细胞和浸入的白细胞表面都有表达的ED1、CD68和主要组织相容性复合体(MHC)抗原。因而梗死后脑组织损伤的形成伴有内源性（小胶质细胞）和外源性（多形核白细胞、中性粒细胞、单核细胞）炎细胞的参与。
目录：
一、脑缺血后炎性细胞的变化
二、炎细胞损伤机制
三、炎细胞与炎性因子
四、炎细胞加重缺血脑损伤的相反观点
五、治疗探讨
参考文献：
1 Yoshimoto T, Houkin K, Tada M, et al. Induction of cytokine, chemokines and adhesion molecule mRNA in a rat forebrain reperfusion model. Acta Neuropathol, 1997, 93:154-158.
2 Oostveen JA, Dunn E, Carter DB,et al. Neuroprotective efficacy and mechanisms of novel pyrrolopyrimidine lipid peroxidation inhibitors in the gerbil forebrain ischemia model. J Cereb Blood Flow Metab, 1998, 18:539-547.
3 Krupinski J, Kaluza J,Kumar P,et al. Immunocytochemical studies of cellular reaction in human ischemic brain stroke. MAB anti-CD68 stains macrophages, astrocytes and microglial cells in infarcted area. Folia Neuropathol, 1996,34:17-24.
4 Lees GJ. The possible contribution of microglia and macrophage to delayed neuronal death after ischemia. J Neurol Sci, 1993, 114:119-122.
5 Stoll G, Jander S, Schroeter M. Inflammation and glial responses in ischemic brain lesions. Prog Neurobiol, 1998,56:149-171.
6 Nawashiro H, Tasaki K,Ruetzler CA,et al. TNF-alpha pretreatment induces protective effects against focal cerebral ischemia in mice. J Cereb Blood Flow Metab, 1997, 17:483-490.
7 Elneihoum AM, Falke P, Axelsson L,et al. Leukocyte activation detected by increased plasma levels of inflammatory mediators in patients with ischemic cerebrovascular di- seases. Stroke, 1996, 27:1734-1738.
8 Akopov SE, Simonian NA, Grigorian GS. Dynamic polymorphonoclear leukocyte accumu- lation in acute cerebral infarction and their correlation with brain tissue damage, Stroke, 1996, 27 : 1739-1743.
9 Fujinuma K,Sakai F,Iizuka T,et al.In-111-labeled leukocyte brain SPECT imaging in acute ischemic stroke in man. Rinsho Shinkeigaku, 1997, 37:13-20.
10 Hayward NJ, Elliott PJ, Sawyer SD,et al. Lack of evidence for neutrophil participation during infarct formation following focal cerebral ischemia in the rat. Exp Neurol, 1996,139:188-202.
11 Kogure K,Yamasaki Y,Matsuo Y,et al. Inflammation of the brain after ischemia. Acta Neurochir, 1996,66 Suppl: 40-43.
12 Tomita M, Fukuuchi Y. Leukocytes, macrophages and secondary brain damage following cerebral ischemia. Acta Neurochir 1996, 66 Suppl: 32-39.
13 Akopov SE, Grigorian GS,Ovanessian GA. Deavtivation of NO by polymorphonuclear leukocyte in patients with ischemic cerebral infarction. Stroke, 1996, 27:2337-2338.
14 Stoll G, Jander S, Schroeter M. Inflammation and glial responses in ischemic brain lesions. Prog Neurobiol, 1998,56:149-171.
15 Matsuo Y, Yamasaki Y, Kogure K. Inflammatory reaction after brain damage and prospective therapy against damage impending cerebral infarction. Keio J Med, 1996, 45:270-274.
16 Yanaka K,Camarata PJ,Spellman SR,et al.Neuronal protection from cerebral ischemia by synthetic fibronectin peptides to leukocyte adhesion molecules. J Cerebral Blood Flow Metab,1996,16:1120-1125.
17 Miasoedova NF, Skvortsova VI, Nasonov EL, et al.Investigation of mechanisms of neuro-protective effect of semax in acute period of ischemic stroke. Zh Nevrol Psikhiatr Im S S Korsakova, 1999,99:15-19.
18 Skvortsova VI, Nasonov EL, Zhuravleva EIu, et al. Clinico-immunobiochemical monitoring of factors of focal inflammation in the acute period of hemispheric ischemic stroke. Zh Nevrol Psikhiatr Im S S Korsakova, 1999,99:27-31.
资料包括： 论文(5页4898字)
说明：
关键词： 脑,缺血损伤,促炎性细胞因子
脑动脉阻断后即使立即再通，脑组织的缺血损伤也不能完全恢复正常，而且不能完全挽救由继发损伤造成的脑缺血组织的继续扩大［1］。缺血后脑死亡的机制可能与组织酸中毒、神经元释放兴奋性氨基酸、细胞内钙聚集、氧化应激（蛋白氧化、脂质过氧化、DNA氧化）、一氧化氮合成、微循环损害及弥散性去极化抑制等有关。目前，较多的研究兴趣集中在缺血再灌注后的炎性过程，缺血细胞以及缺血激活的内皮细胞、白细胞，产生促炎性细胞因子，表达粘附分子，导致白细胞积聚和外流［1］。有些作者认为，缺血后导致细胞死亡的主要因素之一可能是白细胞浸润，甚至提出脑缺血治疗的途径一是再通动脉，二是抑制细胞因子的促炎性作用［2］。现将有关的研究报道综述如下。
一、脑缺血后炎性细胞的变化
1.动物实验的依据：缺血脑组织可检到CD11和CD18阳性浸入的白细胞；OX42免疫反应的向上调节可显示伴形态变化的激活小胶质细胞以及在激活的小胶质细胞和浸入的白细胞表面都有表达的ED1、CD68和主要组织相容性复合体(MHC)抗原。因而梗死后脑组织损伤的形成伴有内源性（小胶质细胞）和外源性（多形核白细胞、中性粒细胞、单核细胞）炎细胞的参与。
目录：
一、脑缺血后炎性细胞的变化
二、炎细胞损伤机制
三、炎细胞与炎性因子
四、炎细胞加重缺血脑损伤的相反观点
五、治疗探讨
参考文献：
1 Yoshimoto T, Houkin K, Tada M, et al. Induction of cytokine, chemokines and adhesion molecule mRNA in a rat forebrain reperfusion model. Acta Neuropathol, 1997, 93:154-158.
2 Oostveen JA, Dunn E, Carter DB,et al. Neuroprotective efficacy and mechanisms of novel pyrrolopyrimidine lipid peroxidation inhibitors in the gerbil forebrain ischemia model. J Cereb Blood Flow Metab, 1998, 18:539-547.
3 Krupinski J, Kaluza J,Kumar P,et al. Immunocytochemical studies of cellular reaction in human ischemic brain stroke. MAB anti-CD68 stains macrophages, astrocytes and microglial cells in infarcted area. Folia Neuropathol, 1996,34:17-24.
4 Lees GJ. The possible contribution of microglia and macrophage to delayed neuronal death after ischemia. J Neurol Sci, 1993, 114:119-122.
5 Stoll G, Jander S, Schroeter M. Inflammation and glial responses in ischemic brain lesions. Prog Neurobiol, 1998,56:149-171.
6 Nawashiro H, Tasaki K,Ruetzler CA,et al. TNF-alpha pretreatment induces protective effects against focal cerebral ischemia in mice. J Cereb Blood Flow Metab, 1997, 17:483-490.
7 Elneihoum AM, Falke P, Axelsson L,et al. Leukocyte activation detected by increased plasma levels of inflammatory mediators in patients with ischemic cerebrovascular di- seases. Stroke, 1996, 27:1734-1738.
8 Akopov SE, Simonian NA, Grigorian GS. Dynamic polymorphonoclear leukocyte accumu- lation in acute cerebral infarction and their correlation with brain tissue damage, Stroke, 1996, 27 : 1739-1743.
9 Fujinuma K,Sakai F,Iizuka T,et al.In-111-labeled leukocyte brain SPECT imaging in acute ischemic stroke in man. Rinsho Shinkeigaku, 1997, 37:13-20.
10 Hayward NJ, Elliott PJ, Sawyer SD,et al. Lack of evidence for neutrophil participation during infarct formation following focal cerebral ischemia in the rat. Exp Neurol, 1996,139:188-202.
11 Kogure K,Yamasaki Y,Matsuo Y,et al. Inflammation of the brain after ischemia. Acta Neurochir, 1996,66 Suppl: 40-43.
12 Tomita M, Fukuuchi Y. Leukocytes, macrophages and secondary brain damage following cerebral ischemia. Acta Neurochir 1996, 66 Suppl: 32-39.
13 Akopov SE, Grigorian GS,Ovanessian GA. Deavtivation of NO by polymorphonuclear leukocyte in patients with ischemic cerebral infarction. Stroke, 1996, 27:2337-2338.
14 Stoll G, Jander S, Schroeter M. Inflammation and glial responses in ischemic brain lesions. Prog Neurobiol, 1998,56:149-171.
15 Matsuo Y, Yamasaki Y, Kogure K. Inflammatory reaction after brain damage and prospective therapy against damage impending cerebral infarction. Keio J Med, 1996, 45:270-274.
16 Yanaka K,Camarata PJ,Spellman SR,et al.Neuronal protection from cerebral ischemia by synthetic fibronectin peptides to leukocyte adhesion molecules. J Cerebral Blood Flow Metab,1996,16:1120-1125.
17 Miasoedova NF, Skvortsova VI, Nasonov EL, et al.Investigation of mechanisms of neuro-protective effect of semax in acute period of ischemic stroke. Zh Nevrol Psikhiatr Im S S Korsakova, 1999,99:15-19.
18 Skvortsova VI, Nasonov EL, Zhuravleva EIu, et al. Clinico-immunobiochemical monitoring of factors of focal inflammation in the acute period of hemispheric ischemic stroke. Zh Nevrol Psikhiatr Im S S Korsakova, 1999,99:27-31.