Nitric oxide mediates the change of proteoglycan synthesis in the human lumbar intervertebral disc in response to hydrostatic pressure.

摘要: Study design This in vitro study clarifies the role of nitric oxide (NO) human lumbar intervertebral disc metabolism. Objective To investigate effects NO on proteoglycan synthesis discs and to test hypothesis that is a mediator changes response hydrostatic pressure. Summary background data The authors have clarified pressure has an apparent effect as well matrix metalloproteinase production disc. cellular mechanisms underlying cells remain be clarified. Herniated produce interleukin (IL)-1 beta. In articular cartilage, mediates change by IL-1 or shear stress. Methods Fifty-eight specimens were obtained from patients who had undergone posterior discectomy. chopped into 1-2-mm cubes incubated plastic syringe with 1 mL Dulbecco's modified Eagle's medium (DMEM). syringes placed water-filled vessel kept at 37 C. Hydrostatic pressures (control), 3, 30 atmospheres (atm) applied. Proteoglycan was determined (35)S-sulfate incorporation rates. Nitrite (the stable oxidation product NO) concentration DMEM spectrophotometric method based Griess reaction. As competitive inhibitor synthases, N(G)-methyl-l-arginine (l-NMA, 10-1000 micromol) organic donor NO, S-nitroso-N-acetylpenicillamine (SNAP, 1-200 used. Results Addition l-NMA suppressed increased rates dose-dependent fashion. SNAP exogenous content significantly Three-atmosphere stimulated Rates approximately 1.3-fold greater than atm, whereas 30-atm inhibited However, hydrostaticpressure inverse production. At 3 decreased slightly relative 1.32-fold atm. L-NMA enhanced 3-atm pressure-induced increase also relieved suppression Conclusion current confirmed previous finding herniated cultures spontaneously NO. Endogenously generated exogenously supplied influenced cells, one mediators These results may show autocrine paracrine play important regulation cell metabolism under mechanical stress pathophysiology degeneration.