The correlation between nitric oxide and vascular endothelial growth factor in spinal cord injury
| Autor: | Serpil Savaş, Irfan Altuntas, Cagri Savas, Ali K. Adiloglu |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Male
Vascular Endothelial Growth Factor A medicine.medical_specialty Free Radicals Endothelium medicine.medical_treatment Central nervous system Arginine Nitric Oxide Nitric oxide Central nervous system disease chemistry.chemical_compound Malondialdehyde Internal medicine medicine Animals Enzyme Inhibitors Rats Wistar Spinal cord injury Spinal Cord Injuries business.industry Growth factor General Medicine medicine.disease Spinal cord Rats Vascular endothelial growth factor NG-Nitroarginine Methyl Ester Endocrinology medicine.anatomical_structure Neurology chemistry Anesthesia Neurology (clinical) Nitric Oxide Synthase business |
| Zdroj: | Spinal Cord. 46:113-117 |
| ISSN: | 1476-5624 1362-4393 |
| DOI: | 10.1038/sj.sc.3102066 |
| Popis: | Prospective, randomized, placebo-controlled, experimental study. The issue of whether nitric oxide (NO) production is beneficial or deleterious on ischemic injuries of the central nervous system still remains doubtful. Vascular endothelial growth factor (VEGF) is known to induce the release of NO from endothelial cells. However, the effect of NO on VEGF synthesis is not clear. We aimed to determine the effects of L-arginine and NG-nitro-L-arginine methyl ester (L-NAME) on VEGF synthesis and free radicals in a rat model of spinal cord ischemia-reperfusion (IR) injury. Surgical Research Laboratory of a Medical School. Twenty-eight Wistar rats were divided into four groups as follows (n=7): Sham, IR injury, L-arginine, and L-NAME. Infrarenal abdominal aorta was occluded to induce spinal cord ischemia. L-Arginine (100 mg/kg) and L-NAME (10 mg/kg) were given before aortic occlusion. Biochemical assays of malondialdehyde (MDA), NO and VEGF were carried out in spinal cord specimens. L-Arginine treatment significantly increased MDA and NO, but decreased VEGF levels in spinal cord. However, nonselective inhibition of NOS with L-NAME significantly decreased MDA and NO, but increased VEGF levels. Besides, the positive linear correlation between MDA and NO, and negative linear correlations between MDA, NO and VEGF levels have also been demonstrated. Nonselective inhibition of NO synthase activity with L-NAME attenuated free radical formation and increased VEGF level when compared with NO precursor L-arginine in a rat model of spinal cord ischemia. We suggest that inhibition of NO synthase, as well as induction of VEGF, may be a therapeutic option in spinal cord IR injury. |
| Databáze: | OpenAIRE |
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