Effect of mechanical stress loaded on the chondrocytes

骨关节病是一种常见的关节退化途径，是由关节软骨上的机械应力引起的。我们先前在体外证明了蛋白激酶C参与了骨关节炎的发生发展。在本研究中，我们在体外研究了机械应力对软骨细胞代谢和蛋白激酶C活性的影响。加载在软骨细胞上的低频率和大小的循环拉伸增加了蛋白多糖的合成。然而，高频率和高强度的胁迫降低了它的合成。在此条件下，蛋白激酶C的活性降低。这些结果表明，蛋白激酶C参与了应激介导的蛋白多糖合成的抑制。我们还研究了一氧化氮在机械应力作用下的变化。两种状态均可抑制NO的合成，提示NO参与了应激引起的软骨细胞代谢改变。

Osteoarthrosis, a common pathway of joint deterioration, is caused by mechanical stress loaded on articular cartilage. We previously demonstrated the involvement of protein kinase C in the development of osteoarthritis in vitro. In the present study, we examined the effect of mechanical stress on chondrocyte metabolism and the activity of protein kinase C in vitro. Low frequency and magnitude of cyclic tensile stretch loaded on chondrocytes increased proteoglycan synthesis. However, high frequency and magnitude of stress decreased its synthesis. In this condition, activity of protein kinase C was reduced. These results suggest an involvement of protein kinase C in the stress mediated inhibition of proteoglycan synthesis. We also investigated the alteration of nitric oxide with mechanical stress. Both conditions caused the inhibition of No synthesis, thereby indicating the involvement of No in stress mediated alteration of the chondrocyte metabolism.