Effects of oxidative stress to pathogenesis of cleft palate.

为探讨氧化应激在腭裂发病机制中的作用，对妊娠小鼠给予TCDD、类固醇、脂多糖和D-氨基半乳糖等氧化应激诱导剂。因此，人们认为只有在DAM(特别是肝脏)内的氧化应激对腭裂的发生没有太大的影响。因此，采用TCDD染毒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记物的低表达，提示TCDD除通过抑制腭部融合的机制外，还可能通过与成骨细胞结合后的裂开和肌肉形成的抑制来诱导腭裂。

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.