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作 者:黄生高[1] 张建兴[1] 熊培颖[1] 王明朗[1]
出 处:《中南大学学报(医学版)》2006年第4期518-522,共5页Journal of Central South University :Medical Science
基 金:湖南省自然科学基金(03JJY4033)
摘 要:目的:研究在持续静压力(continuously compressive pressure,CCP)作用下人牙周膜细胞(hu-man perio donta lligament cells,HPDLCs)核因子КB受体活化因子配体(receptor activator of nuclearfactor kappaB ligand,RANKL)的表达变化,探讨其在正畸性骨改建中的作用机制。方法:用组织块酶消化法原代培养HPDLCs,建立压力模型,分别对细胞施以1,2,3g/cm2顶-底轴向压力0.5,1.5,6,12,24和48h,利用逆转录聚合酶链反应(reverse transcription-polymerase chain reaction,RT-PCR)法检测RANKLmRNA的表达变化。结果:随着CCP作用时间的增加,HPDLCs RANKL表达增强(P<0.01);随力值增加,RANKL mRNA表达增强,力值为2g/cm2时,改变最明显(P<0.05)。结论:CCP可上调HPDLCsRANKLmRNA表达。Objectiv the expression of receptor ligament cells (HPDLCs) e To determine the effect of continuously compressive pressure (CCP) on activator of nuclear factor kappa B ligand (RANKL) in human periodontal and to investigate the role of RANKL in alveolar bone rebuilding during orthodontic tooth movement. Methods The primary HPDLCs were isolated from human periodontal lig- ament by explanting enzymatic digestion with trypsin and collagenase to establish a pressure model. Top-bottom axial pressures ( 1 , 2, and 3 g/cm^2 ) were laid on HPDLCs for 0.5, 1.5, 6, 12, 24, and 48 h, respectively. The RANKL expression was identified by the reverse transcription-polymerase chain reaction ( RT-PCR ) at the mRNA level. Results The expression of RANKL mRNA significantly increased in a time-dependent manner ( P 〈 0.01 ) , so did the value of pressure, especially in the 2 g/cm^2 group ( P 〈 0. 05 ). Conclusion CCP can up-regulate the expression of RANKL mRNA in human periodontal ligament cells.
关 键 词:压力 牙周膜细胞 细胞核因子KB受体活化因子配体 逆转录聚合酶链反应
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