咪唑克生对实验性变态反应性脑脊髓炎干预作用的初步观察

被引：15

作者：

朱振国 ^{[1
]}

郑荣远 ^{[1
]}

陈国钱 ^{[1
]}

韩钊 ^{[1
]}

张磊 ^{[1
]}

殷为勇 ^{[1
]}

周红宇 ^{[2
]}

机构：

[1] 温州医学院第一附属医院

来源：

温州医学院学报 | 2006年 / 01期

基金：

浙江省自然科学基金;

关键词：

脑脊髓炎,自身免疫性,实验性; 咪唑克生; 咪唑啉受体; 动物实验;

D O I：

10.13771/j.cnki.33-1386/r.2006.01.001

中图分类号：

R744.53 [];

学科分类号：

摘要：

目的:探讨不同剂量的咪唑克生(Ida)对Lewis大鼠实验性变态反应性脑脊髓炎(EAE)的影响。方法:采用豚鼠全脊髓匀浆(GPSCH)脚垫皮下注射,免疫Lewis大鼠复制EAE模型,采用量化评分法, 比较不同剂量组咪唑克生对EAE发病率、潜伏期、临床症状和组织学的影响。结果:对照组的发病率为 85．7％(6/7),潜伏期为(11．2±0．45)d。低剂量咪唑克生(2 mg/kg)可降低发病率37．5％(3/8),明显延长潜伏期[(13．05±0．58)d,P<0．05],减轻其临床症状和中枢神经系统(CNS)炎症细胞浸润(P< 0．05),而高剂量咪唑克生(16 mg/kg)对EAE的潜伏期、临床症状和CNS炎症细胞浸润均无影响。结论: 低剂量咪唑克生可减轻Lewis大鼠EAE的炎症细胞浸润、脱髓鞘改变及临床症状,对EAE的发病具有干预(保护)作用。推测这可能与CNS内咪唑啉2受体有关。

引用

页码：1 / 5

页数：5

共 9 条

[1]

Protection of focal ischemic infarction by rilmenidine in the animal: evidence that interactions with central imidazoline receptors may be neuroprotective. Reis DJ,Regunathan S,Golanov EV,et al. The American Journal of Cardiology . 1994

[2]

Prazosin suppresses development of axonal damage in rats inoculated for experimental allergic encephalomyelitis. White SR,Black PC,Samathanam GK,et al. J Neuroimmunol . 1992

[3]

The role of CD8(+) T cells in multiple sclerosis and its animal models. Goverman J,Perchellet A,Huseby ES. Current Cancer Drug Targets . 2005

[4]

Immunocytochemical localization of an imidazoline receptor protein in the central nervous system. Ruggiero DA,Regunathan S,Wang H,et al. Brain Research . 1998

[5]

The alpha 2-adrenoceptor antagonist idazoxan is an agonist at 5-HT1A autoreceptors modulating serotonin synthesis in the rat brain in vivo. Llado J,Esteban S,Garcia-Sevilla JA. Neuroscience Letters . 1996

[6]

Administration of the 5-hydroxytryptamine(1A) receptor antagonist WAY 100635 sup-presses acute experimental allergic encepha lomyelitis in Lewis rats. Freire-Garabal M,Nunez MJ,Balboa J,et al. Neuroscience Letters . 2003

[7]

Two minor determi nants of myelin basic protein induce experimental allergic en cephalomyelitis in SJL/J mice. Kono DH,Urban JL,Horvath SJ,et al. The Journal of Experimental Medicine . 1988

[8]

IL-6 plays a crucial role in the induction phase of myelin oligodendrocyte gluco protein 35-55 induced experimental autoimmune encephalomyelitis. Okuda Y,Sakoda S,Fujimura H,et al. J Neuroimmunol . 1999

[9]

Reduction in focal cerebral ischemia by agents acting at imidazole receptors. Maiese K,Pek L,Berger SB,Reis DJ. Journal of Cerebral Blood Flow and Metabolism . 1992

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