Cyclosporin-A inhibits inducible nitric oxide synthase activity and expression after spinal cord injury in rats

被引：25

作者：

Diaz-Ruiz, A

Vergara, P

Perez-Severiano, FP

Segovia, J

Guizar-Sahagún, G

Ibarra, A

Ríos, C

机构：

[1] Inst Nacl Neurol & Neurocirug, Dept Neuroquim, Mexico City 14269, DF, Mexico

[2] IPN, Ctr Invest & Estudios Avanzados, Dept Fisiol Biofis & Neurociencias, Mexico City, DF, Mexico

[3] Ctr Med Nacl Siglo 21, Hosp Especialidades, Dept Neurociencias, Mexico City, DF, Mexico

[4] Ctr Invest Proyecto Camina, Mexico City, DF, Mexico

来源：

NEUROSCIENCE LETTERS | 2004年 / 357卷 / 01期

关键词：

cyclosporin-A; spinal cord injury; neuroprotection; nitric oxide synthase;

D O I：

10.1016/j.neulet.2003.12.042

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Nitric oxide is generated from L-arginine by a family of three distinct nitric oxide synthase (NOS) enzymes playing a crucial role in the physiopathology of spinal cord injury (SCI). Cyclosporin-A (CsA), an immunosupressive agent, may be used to inhibit the activity of iNOS and perhaps to protect against neural tissue destruction. Rats were submitted to SCI by contusion, and killed 4, 24 and 72 h after lesion. Results showed an increase in the activity of iNOS at 72 h after the SCI, inhibited by CsA (2.5 mg/kg) administered 12 h after trauma. iNOS Western blot assay showed an increase in the expression of iNOS after trauma, also antagonized by CsA administration. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

引用

页码：49 / 52

页数：4

共 20 条

[11] Neurotoxicity of glutamate at the concentration released upon spinal cord injury [J].