Research Article

细胞松弛素D通过p38-MAPK信号通路促进MC3T3-E1细胞成骨分化

卷 20, 期 1, 2020

页: [79 - 88] 页: 10

弟呕挨: 10.2174/1566524019666191007104816

open access plus

摘要

背景:外伤,肿瘤切除,感染或先天性畸形引起的骨缺损是一种常见的临床疾病。骨组织工程被认为是骨缺损重建的一种有前途的方法。因此,可以促进成骨作用的药物受到极大关注。细胞松弛素D(Cyto D)是一种来自霉菌的代谢产物,被证明能够修饰肌动蛋白,重组细胞骨架,然后促进成骨分化。 目的:本研究旨在探讨Cyto D对小鼠成骨前MC3T3-E1细胞成骨分化的影响及其机制。 方法:探讨细胞色素D的最佳浓度。通过碱性磷酸酶(ALP)染色,茜素红S(ARS)染色,Western印迹和定量实时聚合酶链反应(RT-qPCR)评估了Cyto D诱导的MC3T3-E1细胞的成骨分化。另外,利用特异性途径抑制剂来探索MAPK途径是否参与该过程。 结果:结果表明,最佳作用浓度为10-2μg/ ml。补充Cyto D可上调Runx2,OCN和OSX的表达。p38蛋白的ALP活性,钙沉积和磷酸化水平也得到改善。抑制该途径显着降低了p38的激活以及成骨相关基因的表达。 结论:Cyto D可通过p38-MAPK信号通路促进MC3T3细胞的成骨分化,但不能促进ERK1 / 2或JNK的表达,是改善MC3T3细胞成骨性的潜在药物。

关键词: 骨重塑,细胞松弛素D,成骨分化,MC3T3-E1细胞,MAPK,p38。

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