| [Backgrouds] Emerging novel strategies of SCI treatments are based on the selective regulation of specific targets, which are involved in the process of occurrence and progression of SCI. Different expression levels of NOS were correlated to the degree of secondary injury of SCI. The secondary injury could be ameliorated by different inhibitors of NOS. NOS could be regarded as a target of treatment of SCI and have been used in experimental studies. Now genes of NOS were definited in many species of animals and tissues. It have been proved that oligodeoxynucleotides could inhibited target genes specially.[Objectives] Firstly, to study the distributive and expressive laws of three different nitric oxide synthases(iNOS, nNOS and eNOS) in spinal cord injury. Secondly, to study the changes and significance of the apoptosis and p38 mitogen activated protein kinase (MAPK) transduction way after spinal cord injury. Thirdly, to study the influences of antisense oligodeoxynucleotide (ASODN) of iNOS and nNOS on the apoptosis percentage and the neural function recovery after spinal cord injury.[Methods] The spine of rats were compressed with the Nystrom's methods. The first part of rats were used to study the the distributive and expressive laws of three different nitric oxide synthases in spinal cord tissues in 6, 12, 24, 48 and 72 hours by immunohistochemistrical and image analysis methods. The morphology of apoptosis was studied with transmission electron microscopy (TEM). In the second part, the changes of p38MAPK signal transduction way detected by Westrn blotting method. SB203580, the specific inhibitor of p38MAPK, were injected into the subarachnoid space by the micro-injection immediately after the compressive injury of the spinal cord. Westrn blotting was used to detect the changes of p38MAPK signal transduction way at the time point of Omin, 30min, 6h, 24h and 72h after injury. According to the upper studies, in the third part of rats, ASODN-iNOSand ASODN-nNOS were microinjected into spinal subarachnoid space 12 hours before the rat's spinal cord injured. Then the injured spinal cord tissues were gained and divided into several parts, one for RT-PCR test to detect the change of mRNA of NOS and the other for flow cytometry (FCM) to detect the percentages of apoptosis of neural cells at 72h after the spinal cord injury. The content of nitric oxide (NO) and activity of nitric oxide synthase (NOS) were detected by spectrophotography. The neural functional recovery was evaluated with animal praxiology, electrical physiological detection, magnetic resonance imaging. The pathology of spinal cord tissues were studied by HE and Nissl staining methods.[Results] The positive areas were localized in cellplasm with brown stained. These cells belong to anterior horn, central canal and posterior horn. There was always expression of nNOS before and after spinal cord injury. This expression was continuing and little changed. On the contrary iNOS were not expressed in normal control group but expressed in every injured groups. After injury the expression of iNOS improved quickly to the top point in 12-48 hours and then dropped gradually. There were obviously difference between 12~48 hours and the normal control group (p<0.05). There was not exactly expression of eNOS in normal and injuried spinal cord tissues. There was obvious change of p38 MAPK after spinal cord injury. The kinase appeared at 30min, topped at 6h and then went down gradually. When SB203580 was used the active level of p38MAPK, the content of NO, the activity of NOS and the percentage of apoptosis were decreased respectively (p<0.05). ASODN-iNOS and ASODN-nNOS could suppress the expression of mRNA-iNOS/nNOS, the content of NO, the activity of NOS and and the apoptosis percentage of neural cells respectively (p<0.01 and 0.05). Both ASODN-iNOS and ASODN-nNOS could improve neural functions after SCI but the former was better than the latter. Neither NSODN-iNOS nor NSODN-nNOS had any above roles.[Conclusions] Firstly, the mainly expressions of NOS in spin...
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