摘要
目的在P1代1月龄雄性新西兰大白兔膝关节软骨细胞水平,观察周期性张应变(CTS)对重组白细胞介素(IL)-1β诱导的一氧化氮(NO)表达的拮抗作用,从而了解力学信号在软骨修复中的活动机制。方法将体外培养的兔膝关节P1代软骨细胞随机分为5组,每组有18个样本,分为空白对照组、IL-1β作用组及IL-1β和CTS共同作用组,CTS分别作用8、16、24h,24h后收取培养细胞上清液测定NO含量,比较各组变化。结果正常兔膝关节P1代软骨细胞表达一定量的NO,IL-1β作用组NO含量明显升高,差异具有统计学意义(P<0.05);IL-1β和CTS共同作用组NO含量明显减低,同IL-1β作用组相比,各组间差异具有统计学意义(P<0.05),CTS作用8h最佳阻止了NO的表达。结论CTS对rhIL-1β诱导的NO表达具有强大的拮抗作用,并且CTS产生的力学信号转化成强大的生物化学信号后能够持续性地以特定方式阻滞分解介质的产生。
Objective To observe the effects of cyclic tensile strain （CTS） on rhIL-1β induced expression of nitile oxide （NO） in chondrocytes from one month old male rabbits, and to understand the mechanisms of mechanical signaling in cartilage repair. Methods Rabbit articular chondrocytes were cultured in vitro and randomly divided into 5 groups, namely, the control group, rhIL-1β group, and rhIL-1β ＋ CTS groups, with 18 samples in each. The rhIL-1β ＋ CTS groups were subjected to treatment with CTS for 8 h, 16 h and 24 h, respectively. After 24 hours, the supernatant of each group of cell culture was collected. The level of NO in the suparnatant was compared across these groups. Results Expression of NO was found in normal rabbit chondrocytes, and was significantly enhanced with ad- dition of rhIL-1β（P〈0.05）. The level of NO was obviously lower in groups with rhIL-1β and CTS, compared with that in the group rhIL-1β（P〈0.05）. Maximal inhibition of NO expression was achieved with 8 hours of CTS incubation. Conclusion CTS can greatly inhibit the expression of NO induced by rhIL-1β. Signals generated by CTS were converted into potent biochemical events that may block the synthesis of catabolic mediators in a persistent manner.
出处
《中国药物与临床》
CAS
2009年第4期265-267,共3页
Chinese Remedies & Clinics
基金
国家自然科学基金(30872616)
山西省归国留学人员重点科研项目(200605)
