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作 者:赵一松 钟慧敏 何志伟[2] 张国梁[3] 吴江[3]
机构地区:[1]天津市滨海新区塘沽口腔医院,天津300450 [2]哈尔滨医科大学附属第二临床医学院,黑龙江哈尔滨150001 [3]佳木斯大学附属口腔医院,黑龙江佳木斯154002
出 处:《上海口腔医学》2015年第1期56-60,共5页Shanghai Journal of Stomatology
摘 要:目的:探索p38信号通路在上颌突间充质细胞体外成骨分化中的调控作用。方法:取第1代E12.5 d的小鼠上颌突间充质细胞进行成骨诱导培养1周,实验组加入SB203580(p38磷酸化抑制剂)。通过免疫荧光检测磷酸化p38的表达,通过Brdu标记和免疫荧光检测细胞的增殖能力,通过ALP染色和定量PCR检测成骨标志物的表达。采用SPSS18.0软件包对数据进行统计学分析。结果 :成骨诱导可促进上颌突间充质细胞中p38的磷酸化(p-p38)。抑制p38的磷酸化,可抑制上颌突间充质细胞增殖,降低成骨标志物ALP、Runx2、OCN和OPN的表达,使ALP染色减弱。结论:p38信号通路参与调控体外培养的上颌突间充质细胞的成骨分化。PURPOSE: To explore whether p38 signal pathway regulates osteogenic differentiation of maxillary primordium mesenchymal cells. METHODS: The first passage of maxillary primordium mesenchymal cells(MPMCs) from E12.5 embryos were cultured in the osteogenic medium, and 10 n M SB203580(an inhibitor of phosphorylation of p38) was added in the medium in the experimental group for 1 week. Then immunofluorescence staining was applied to detect the phosphorylation of p38 in MPMCs. Brdu label and immunofluorescence staining were used to detect the proliferation of MPMCs. ALP staining and q PCR were used to detect the m RNA expression of ALP, Runx2, OCN and OPN in MPMCs.ALP staining and PCR were used to evaluate the osteogenic capability of MPMCs. SPSS 18.0 software package was used to analyze the data. RESULTS: Osteogenic induction could promote phosphorylation of p38, inhibit phosphorylation of p38 and proliferation of MPMCs, down-regulate the expression of ALP, Runx2, OCN and OPN, thus weaken the ALP staining in MPMCs. CONCLUSIONS: p38 signal pathway regulates osteogenic differentiation of MPMCs in vitro.
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