Hennerbichler Alfred, Fermor Beverley, Hennerbichler Diana, Weinberg J Brice, Guilak Farshid
Department of Surgery, Division of Orthopaedic Surgery, Duke University Medical Center, Box 3093, 375 Medical Sciences Research Building, Durham, NC 27710, USA.
Biochem Biophys Res Commun. 2007 Jul 13;358(4):1047-53. doi: 10.1016/j.bbrc.2007.05.026. Epub 2007 May 14.
Injury or loss of the knee meniscus is associated with altered joint stresses that lead to progressive joint degeneration. The goal of this study was to determine if dynamic mechanical compression influences the production of inflammatory mediators by meniscal cells. Dynamic compression increased prostaglandin E2 (PGE(2)) and nitric oxide (NO) production over a range of stress magnitudes (0.0125-0.5 MPa) in a manner that depended on stress magnitude and zone of tissue origin. Inner zone explants showed greater increases in PGE(2) and NO production as compared to outer zone explants. Meniscal tissue expressed NOS2 and NOS3 protein, but not NOS1. Mechanically induced NO production was blocked by NOS inhibitors, and the non-selective NOS inhibitor L-NMMA augmented PGE(2) production in the outer zone only. These findings suggest that the meniscus may serve as an intra-articular source of pro-inflammatory mediators, and that alterations in the magnitude or distribution of joint loading could significantly influence the production of these mediators in vivo.
膝关节半月板损伤或缺失与关节应力改变相关,进而导致关节进行性退变。本研究的目的是确定动态机械压缩是否会影响半月板细胞炎性介质的产生。在一系列应力幅度(0.0125 - 0.5 MPa)范围内,动态压缩以依赖于应力幅度和组织起源区域的方式增加了前列腺素E2(PGE₂)和一氧化氮(NO)的产生。与外侧区外植体相比,内侧区外植体的PGE₂和NO产生增加更为明显。半月板组织表达NOS2和NOS3蛋白,但不表达NOS1。机械诱导的NO产生被NOS抑制剂阻断,非选择性NOS抑制剂L - NMMA仅在外周区增加了PGE₂的产生。这些发现表明,半月板可能作为关节内促炎介质的来源,并且关节负荷大小或分布的改变可能会显著影响这些介质在体内的产生。