THE ROLE OF NITRIC OXIDE DURING THE PROCESS OF INTERVERTEBRAL DISC DEGENERATION AND PREVENTION OF DISC DEGENERATION USING i-NOS ANTI SENSE OLIGONUCLEOTIDE

腰椎间盘退变是引起腰椎间盘功能障碍和下腰痛的主要原因。已知有许多因素会影响椎间盘退变。一氧化氮(NO)是一种无机、气态自由基，被认为是难以捉摸的血管松弛因子。我们已经阐明了NO在椎间盘代谢中的作用，以及i-NOS反义寡核苷酸对实验性兔椎间盘退变模型的预防作用。退变的兔椎间盘自发产生NO和NO，抑制蛋白多糖的合成，增加基质金属蛋白酶-3的生成。I-NOS反义寡核苷酸抑制蛋白多糖丢失和基质金属蛋白酶的产生，组织学上抑制退变过程中藏红素-O染色的减少和纤维环撕裂的产生。

The intervertebral disc degeneration is the major cause of disc dysfunction and low back pain. Many factors are known to influence intervertebral disc degeneration. Nitric Oxide (NO) is an inorganic, gaseous free radical and identified as the elusive blood vessel relaxing factor. We have clarified that the role of NO in disc metabolism and the effects of i-NOS anti-sense oligonucleotide that control NO production to prevent experimental rabbit disc degeneration model. The degenerated rabbit intervertebral disc spontaneously produced NO and NO inhibited proteoglycan synthesis and increased the production of Matrix metalloproteinase-3 in the disc. I-NOS anti-sense oligonucleotide inhibited proteoglycan loss and matrix metalloproteinase production.Histologically, i-NOS anti-sense oligonucleotide inhibited the reduction of Safranin-O staining and production of annulus fibrosus tear during the degeneration process.