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通过水溶性一氧化碳释放分子(CORM)-A1 预防实验性变应性脑脊髓炎(EAE)中蛋白脂质蛋白(PLP)诱导的临床和组织学征象。

Prevention of clinical and histological signs of proteolipid protein (PLP)-induced experimental allergic encephalomyelitis (EAE) in mice by the water-soluble carbon monoxide-releasing molecule (CORM)-A1.

机构信息

Department of Biomedical Sciences, School of Medicine, University of Catania, Italy.

出版信息

Clin Exp Immunol. 2011 Mar;163(3):368-74. doi: 10.1111/j.1365-2249.2010.04303.x. Epub 2011 Jan 14.

DOI:10.1111/j.1365-2249.2010.04303.x
PMID:21235533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3048621/
Abstract

We have evaluated the effects of the carbon monoxide-releasing molecule CORM-A1 [Na(2) (BH(3) CO(2) ); ALF421] on the development of relapsing-remitting experimental allergic encephalomyelitis (EAE) in SJL mice, an established model of multiple sclerosis (MS). The data show that the prolonged prophylactic administration of CORM-A1 improves the clinical and histopathological signs of EAE, as shown by a reduced cumulative score, shorter duration and a lower cumulative incidence of the disease as well as milder inflammatory infiltrations of the spinal cords. This study suggests that the use of CORM-A1 might represent a novel therapeutic strategy for the treatment of multiple sclerosis.

摘要

我们评估了一氧化碳释放分子 CORM-A1 [Na(2) (BH(3) CO(2) ); ALF421] 对 SJL 小鼠实验性自身免疫性脑脊髓炎(EAE)复发缓解型多发性硬化症(MS)模型发展的影响。数据显示,CORM-A1 的长期预防性给药可改善 EAE 的临床和组织病理学征象,表现为累积评分降低、病程缩短和疾病累积发生率降低,以及脊髓炎症浸润减轻。本研究表明,CORM-A1 的应用可能代表多发性硬化症治疗的一种新的治疗策略。

相似文献

1
Prevention of clinical and histological signs of proteolipid protein (PLP)-induced experimental allergic encephalomyelitis (EAE) in mice by the water-soluble carbon monoxide-releasing molecule (CORM)-A1.通过水溶性一氧化碳释放分子(CORM)-A1 预防实验性变应性脑脊髓炎(EAE)中蛋白脂质蛋白(PLP)诱导的临床和组织学征象。
Clin Exp Immunol. 2011 Mar;163(3):368-74. doi: 10.1111/j.1365-2249.2010.04303.x. Epub 2011 Jan 14.
2
Lymphocytes from SJL/J mice immunized with spinal cord respond selectively to a peptide of proteolipid protein and transfer relapsing demyelinating experimental autoimmune encephalomyelitis.用脊髓免疫的SJL/J小鼠的淋巴细胞对蛋白脂质蛋白的一种肽产生选择性反应,并传递复发性脱髓鞘实验性自身免疫性脑脊髓炎。
J Immunol. 1991 Jan 1;146(1):101-7.
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Treatment of relapsing autoimmune encephalomyelitis with T cell receptor V beta-specific antibodies when proteolipid protein is the autoantigen.当蛋白脂蛋白作为自身抗原时,用T细胞受体Vβ特异性抗体治疗复发性自身免疫性脑脊髓炎。
J Neurosci Res. 1996 Jul 15;45(2):104-16. doi: 10.1002/(SICI)1097-4547(19960715)45:2<104::AID-JNR3>3.0.CO;2-E.
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本文引用的文献

1
Specific and strain-independent effects of dexamethasone in the prevention and treatment of experimental autoimmune encephalomyelitis in rodents.地塞米松在预防和治疗实验性自身免疫性脑脊髓炎中的特异性和株系独立性作用。
Scand J Immunol. 2010 Nov;72(5):396-407. doi: 10.1111/j.1365-3083.2010.02451.x.
2
The therapeutic potential of carbon monoxide.一氧化碳的治疗潜力。
Nat Rev Drug Discov. 2010 Sep;9(9):728-43. doi: 10.1038/nrd3228.
3
Update on the treatment options for multiple sclerosis.多发性硬化症的治疗选择更新。
Expert Rev Clin Immunol. 2010 Jan;6(1):77-88. doi: 10.1586/eci.09.75.
4
The CO-releasing molecule CORM-3 protects against articular degradation in the K/BxN serum transfer arthritis model.CO 释放分子 CORM-3 可防止 K/BxN 血清转移关节炎模型中的关节降解。
Eur J Pharmacol. 2010 May 25;634(1-3):184-91. doi: 10.1016/j.ejphar.2010.02.028. Epub 2010 Feb 23.
5
Effects of carbon monoxide releasing molecule-liberated CO on severe acute pancreatitis in rats.一氧化碳释放分子释放的一氧化碳对大鼠重症急性胰腺炎的影响。
Cytokine. 2010 Jan;49(1):15-23. doi: 10.1016/j.cyto.2009.09.013. Epub 2009 Nov 8.
6
Heme oxygenase-1/carbon monoxide: from metabolism to molecular therapy.血红素加氧酶-1/一氧化碳:从代谢到分子治疗
Am J Respir Cell Mol Biol. 2009 Sep;41(3):251-60. doi: 10.1165/rcmb.2009-0170TR. Epub 2009 Jul 17.
7
Overexpression of HO-1 protects against TNF-alpha-mediated airway inflammation by down-regulation of TNFR1-dependent oxidative stress.HO-1的过表达通过下调TNFR1依赖性氧化应激来保护机体免受TNF-α介导的气道炎症。
Am J Pathol. 2009 Aug;175(2):519-32. doi: 10.2353/ajpath.2009.090016. Epub 2009 Jul 16.
8
CORM-3-derived CO modulates polymorphonuclear leukocyte migration across the vascular endothelium by reducing levels of cell surface-bound elastase.源自CORM-3的一氧化碳通过降低细胞表面结合的弹性蛋白酶水平来调节多形核白细胞穿过血管内皮的迁移。
Am J Physiol Heart Circ Physiol. 2009 Sep;297(3):H920-9. doi: 10.1152/ajpheart.00305.2009. Epub 2009 Jun 26.
9
Protective effects of inhaled carbon monoxide in pig lungs during cardiopulmonary bypass are mediated via an induction of the heat shock response.吸入一氧化碳对猪体外循环期间肺的保护作用是通过诱导热休克反应介导的。
Br J Anaesth. 2009 Aug;103(2):173-84. doi: 10.1093/bja/aep087. Epub 2009 Apr 29.
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Heme-oxygenase-1 induction and carbon monoxide-releasing molecule inhibit lipopolysaccharide (LPS)-induced high-mobility group box 1 release in vitro and improve survival of mice in LPS- and cecal ligation and puncture-induced sepsis model in vivo.血红素加氧酶-1的诱导及一氧化碳释放分子在体外抑制脂多糖(LPS)诱导的高迁移率族蛋白B1释放,并在体内脂多糖和盲肠结扎穿刺诱导的脓毒症模型中提高小鼠存活率。
Mol Pharmacol. 2009 Jul;76(1):173-82. doi: 10.1124/mol.109.055137. Epub 2009 Apr 14.