Effects of oxidative stress to pathogenesis of cleft palate.

为了研究氧化应激在腭裂发病机制中的作用，将一些氧化应激诱导剂，即TCDD、类固醇、LPS和D-半乳糖胺，给予妊娠小鼠。因此，认为氧化应激仅在母体（特别是肝脏）内对腭发育没有太大影响。因此，使用TCDD给药小鼠作为氧化应激模型。由于成骨相关蛋白和成肌细胞分化标志物的低表达，提示TCDD可通过腭愈合后的裂开、成骨和成肌抑制以及腭融合抑制的机制诱导腭裂。

To examine effect of the oxidative stress in the cleft palate pathogenesis, some oxidative stress inducers, i.e. TCDD, steroid, LPS, and D-galactosamine, were administered to pregnant mice. As a result, it was thought that palatogenesis was not received much effect by the oxidative stress only within the dam (liver in particular). Therefore TCDD administration mice were used as oxidative stress model. Because underexpression of osteogenesis-related protein and the myoblastic differentiation marker was observed, it was suggested that TCDD can induce cleft palate by dehiscence after the palate union with osteo-, and myogenesis suppression, in addition by the mechanism of palatal fusion inhibition.