Mechanical stress loaded on chondrocytes and cellular apoptosis: involvement of reactive oxygen species.

骨关节病是一种常见的关节恶化途径，当关节组织上的机械应力与这些组织承受该应力的能力之间存在生理失衡时，就会导致骨关节病。虽然已知机械应力是调节软骨代谢的一个重要因素，但涉及的确切机制尚未确定。为了在细胞水平上研究导致软骨退化的潜在机制，我们引入了一种计算机化的压力操作装置(Flexpercell Spline Unit.)来诱导软骨细胞变形。我们发现，当对软骨细胞施加低频率和大小的周期性拉伸时，增加了蛋白多糖(PG)的合成，而高频和大小的应力减少了其合成。一氧化氮(NO)参与了骨关节炎的发病机制。对软骨细胞施加周期性拉伸可明显促进PG和NO的合成。当NO的生成受到抑制时，PG的合成进一步增强。这些数据表明，应激介导的PG合成变化受NO产生的调节。

Osteoarthrosis, a common pathway to joint deterioration, results when a physiological imbalance exists between mechanical stress on the joint tissues and the ability of those tissues to withstand that stress. Although mechanical stress is known to be an essential factor in the regulation of cartilage metabolism, the precise mechanisms involved have not yet been determined. To examine, at the cellular level, the underlying mechanisms that lead to cartilage degradation, we introduced a computerized, pressure-operated device (Flexercell Strain Unit) to induce deformation of chondrocytes. We found that while a low frequency and magnitude of cyclic tensile stretch applied to chondrocytes increased proteoglycan (PG) synthesis, a high frequency and magnitude of stress decreased its synthesis.Nitric oxide (NO) has been implicated in the pathogenesis of OA. Enhanced PG and NO synthesis were evident when cyclic tensile stretch was applied to chondrocytes. When NO production was inhibited, PG synthesis was enhanced further. These data suggest that stress-mediated alteration in PG synthesis was modulated by NO production.