中文摘要：

目的 探讨周期性压力对兔软骨细胞增殖、凋亡和Bcl-2、Bax基因表达的影响.方法 体外分离培养兔关节软骨细胞,在培养液中加入肿瘤坏死因子（TNF）-α模拟骨关节炎（OA）炎症环境,施加172 kPa,2 Hz周期性压力.以细胞增殖及细胞毒性定量检测试剂盒检测软骨细胞增殖情况,流式细胞仪测定软骨细胞凋亡率,逆转录-聚合酶链反应（RT-PCR）测定Bcl-2、Bax基因相对表达量.结果 炎症环境中兔软骨细胞增殖能力降低、细胞凋亡增加,Bcl-2/Bax基因比值降低.对炎症环境中兔软骨细胞施加周期性压力后,细胞增殖能力增强、细胞凋亡减少,Bcl-2/Bax基因比值升高.结论 周期性压力在OA炎症环境中刺激兔软骨细胞,能增加软骨细胞增殖能力,抑制凋亡.其机制可能与上调Bcl-2/Bax基因表达比例有关,为临床上利用生物力学方法治疗OA提供新思路.

英文摘要：

Objective To investigate the influence of periodic pressure on the oliferation/apoptosis and Bcb2/Bax geneexpression in rabbit chondrocytes. Methods Rabbit articular cartilage cells were isolated and cultured in vitro. Add tumor necrosisfactor （TNF） a to simulate inflammation status, and then the cells were given a periodic pressure of 172 kPa, 2 Hz. After beingintervened, rabbit chondrocytes proliferation was detected by live/dead cell vitality assay, and chondrocytes apoptosis rate wastested by flow cytometry. The Bcb2/Bax gene nffNA expression was determined by reverse transcriptiowpolymerase chainreaction （RT-PCR）. Results Rabbit chondrocytes proliferation was inhibited while apoptotic rate increased, Bel 2/Bax gene ratiowas raised in the environment of inflammation, and such situation could be reversed after intervene by the periodic pressure.Conclusions After being intervened with a periodic pressure, the proliferation capacity of rabbit chondrocytes under inflammationcondition was enhanced and cell apoptosis was inhibited. The mechanism may be related to the up-regulated expression of Bcl-2/Bax gene, which may provide new information to clinical therapy of osteoarthritis by biomechanics.