Cyclosporin-A Inhibits Constitutive Nitric Oxide Synthase Activity and Neuronal and Endothelial Nitric Oxide Synthase Expressions after Spinal Cord Injury in Rats |
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Authors: | Araceli?Diaz-Ruiz Paula?Vergara Francisca?Perez-Severiano Jose?Segovia Gabriel?Guizar-Sahagún Antonio?Ibarra Email author" target="_blank">Camilo?RíosEmail author |
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Institution: | (1) Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suarez, S.S.A., México;(2) Departamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del IPN, México;(3) Unidad de Investigación Médica en Enfermedades Neurológicas,Hospital de Especialidades, Centro Médico Nacional Siglo XXI, México;(4) Centro de Investigación del Proyecto Camina, A.C., México;(5) Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía, Av. Insurgentes Sur 3877, Mexico, D.F., Mexico, 14269 |
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Abstract: | Nitric oxide (NO) plays a role in the pathophysiology of spinal cord injury (SCI). NO is produced by three types of nitric oxide synthase (NOS) enzymes: The constitutive Ca2+/calmodulin-dependent neuronal NOS (nNOS) and endothelial NOS (eNOS) isoforms, and the inducible calcium-independent isoform (iNOS). During the early stages of SCI, nNOS and eNOS produce significant amounts of NO, therefore, the regulation of their activity and expression may participate in the damage after SCI. In the present study, we used Cyclosporin-A (CsA) to further substantiate the role of Ca-dependent NOS in neural responses associated to SCI. Female Wistar rats were subjected to SCI by contusion, and killed 4 h after lesion. Results showed an increase in the activity of constitutive NOS (cNOS) after lesion, inhibited by CsA (2.5 mg/kg i.p.). Western blot assays showed an increased expression of both nNOS and eNOS after trauma, also antagonized by CsA administration. |
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Keywords: | Cyclosporin-A neuroprotection nitric oxide nitric oxide synthase spinal cord injury |
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