论文部分内容阅读
为了探索丙二醛(malonaldehyde,MDA)抑制间充质干细胞(mesenchymal stem cells,MSCs)成骨分化的作用机制,用不同浓度的丙二醛孵育MSCs,进行成骨诱导培养,检测碱性磷酸酶活性和钙结节形成;并检测p38和JNK表达水平和磷酸化程度,用这两种信号分子的特异性阻断剂进行验证.结果发现,丙二醛浓度依赖性地降低MSCs碱性磷酸酶的活性,抑制钙结节的形成;并引起p38和JNK的表达上调和磷酸化增强,诱导JNK由胞浆向胞核转位;p38和JNK阻断剂对丙二醛的上述效应有拮抗作用.结果表明,丙二醛可抑制MSCs的成骨诱导分化,其作用机制涉及p38和JNK信号通路的参与.
In order to explore the mechanism of malonaldehyde (MDA) inhibiting the osteogenic differentiation of mesenchymal stem cells (MSCs), MSCs were incubated with different concentrations of malondialdehyde (MDA) to induce osteoblasts. The activities of alkaline phosphatase Activity and calcium nodule formation.P38 and JNK expression levels and phosphorylation were detected by specific inhibitors of these two signaling molecules.It was found that MDA decreased concentration-dependently the activity of alkaline phosphatase , Inhibit the formation of calcium nodules, and cause the up-regulation of p38 and JNK phosphorylation, and induce the translocation of JNK from cytoplasm to nucleus. The antagonistic effect of p38 and JNK blockers on the above effects of malondialdehyde The results showed that MDA could inhibit the osteogenic differentiation of MSCs, and its mechanism of action involved in the involvement of p38 and JNK signaling pathways.