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目的:研究机械牵张力诱导成骨细胞OPG/RANKL表达变化的信号转导途径。方法:在MC3T3-E1细胞加力前半小时加入放线菌酮、吲哚美辛、染料木黄酮、PD098059等抑制剂,通过自制的多通道细胞牵张应力加载系统对细胞施加18%的机械牵张力,细胞的加载作用时间为24h。用RT-PCR方法检测细胞受力前后OPG/RANKL mRNA表达的变化,并进行统计分析。结果:吲哚美辛及染料木黄酮可抑制机械牵张力诱导的MC3T3-E1细胞OPG mRNA表达增加;PD098059可抑制机械牵张力诱导的MC3T3-E1细胞RANKL mRNA表达减少。结论:机械牵张力诱导的OPG表达增加可能是通过环氧合酶或者前列腺素合成途径,也可能是通过酪氨酸磷酸化途径,机械牵张力诱导RANKL表达的减少可能是通过ERK-MAPK途径。
OBJECTIVE: To study the signal transduction pathway of OPG / RANKL expression induced by mechanical stretch in osteoblasts. METHODS: Cycloheximide, indomethacin, genistein and PD098059 were added into MC3T3-E1 cells for half an hour before force, and 18% mechanical force was applied to the cells by self-made multi-channel cell stretch stress loading system Tension, cell loading time for 24h. The changes of OPG / RANKL mRNA expression before and after cell stress were detected by RT-PCR and statistical analysis was made. Results: Indomethacin and genistein inhibited the increase of OPG mRNA expression in MC3T3-E1 cells induced by mechanical strain. PD098059 inhibited the decrease of RANKL mRNA expression in MC3T3-E1 cells induced by mechanical strain. CONCLUSIONS: Mechanical stretch-induced increase of OPG expression may be through the pathway of cyclooxygenase or prostaglandin synthesis or through the tyrosine phosphorylation pathway. The decrease of RANKL expression induced by mechanical strain may be through the ERK-MAPK pathway.