褪黑素信号通路对青少年特发性脊柱侧凸软骨细胞增殖的影响

The effect of melatonin on the proliferation of chondrocytes in the growth plate of the adolescent idiopathic scoliosis patients

中文关键词:  青少年特发性脊柱侧凸  褪黑素  增殖  软骨细胞

英文关键词:Adolescent idiopathic scoliosis  Melatonin  Proliferation  Growth plate chondrocytes

中文摘要:

  【摘要】 目的：检测褪黑素对青少年特发性脊柱侧凸（adolescent idiopathic scoliosis，AIS）患者软骨细胞增殖的影响，并探讨其与AIS病因学的关系。方法：选取2009年1月～2010年12月在我院手术治疗的15例AIS患者（AIS组）和6例非脊柱侧凸患者（对照组）的软骨组织（髂软骨或棘突软骨）行软骨细胞培养。取P2代细胞分别用浓度为0M、10-11M、10-9M、10-7M、10-5M褪黑素连续刺激3d。加入Brdu 12h后用ELLSA法标记，显色后在酶标仪450nm波长下检测光密度（optical density，OD）值以评估软骨细胞的增殖情况。结果：不同浓度（10-11M、10-9M、10-7M、10-5M）褪黑素刺激以后，对照组软骨细胞的OD值分别增加了（5.7±6.7）%、（32.1±11.1）%、（57.5±11.9）%、（103.2±16.2）%（P<0.05）。AIS组软骨细胞的OD值相分别增加了（-0.3±22.3）%、（5.8±29.9）%、（12.7±36.1）%、（10.2±44.0）%（P>0.05）。结论：褪黑素可以有效促进正常软骨细胞增殖，但是却无法有效促进AIS患者软骨细胞的增殖，说明AIS患者中褪黑素信号通路调节软骨内成骨的过程可能存在异常。

英文摘要:

  【Abstract】 Objectives：To identify the effect of melatonin on the proliferation of chondrocytes in the growth plate of adolescent idiopathic scoliosis(AIS) patients，and to explore the role of melatonin in the etiopathogenesis of AIS. Methods: The chondrocytes derived from iliac growth plate of 15 AIS patients and 6 controls were cultured in monolayer and passaged. The growth plate chondrocytes at the end of second passage were cultured with melatonin for 3 consecutive days and reached the final concentration of 0M, 10-11M, 10-9M, 10-7M, 10-5M. The chondrocytes proliferation was investigated based on ELLSA after the cells incubated with Brdu for 12 hours. Optical density(OD) value was measured by microplate reader at the wavelength of 450nm. Results: After the treatment of melatonin, the OD value of the normal growth plate chondrocytes increased by (5.7±6.7)%, (32.1±11.1)%, (57.5±11.9)%, (103.2±16.2)%(P<0.05) respectively, and the OD value of the AIS growth plate chondrocytes increased by (-0.3±22.3)%, (5.8±29.9)%, (12.7±36.1)%, (10.2±44.0)%(P>0.05) respectively. Conclusions: The proliferation of chondrocytes of growth plate can be promoted by melatonin in the normal group but not in the AIS group, which suggests that the abnormal process of endochondral ossification regulated by the melatonin may contribute to the onset and progression of AIS.