地塞米松诱发小鼠腭裂时AnnexinⅠ、cPLA2和PCNA表达的研究

目的 检测膜联蛋白(Annexin Ⅰ)、胞质磷腊酶A2(cytosolic phospholipase A2,cPLA2)、增殖细胞枝抗原(proliferating cell muclear antigen,PCNA)在地塞米松诱导小鼠腭裂腭胚突中的表达变化情况。探讨腭裂的发生机制和预防方法。方法 A/J和C57BL/6j受孕小鼠随机分为正常对照组、地塞米松致畸组（DEX组）、VitB12致畸拮抗组(DE Vit组)和VitB12组。应用蛋白质免疫印迹的方法检测Annexin 0281、cPLA2和PCNA的相对含量。结果 A／J小鼠中，在正常对照组中，随着腭胚突的发育，Annexin Ⅰ表达逐渐升高，其余各实验组也呈相似变化。在DEX组和DEX VitB12组中， AnnexinⅠ的表达明显较对照组和VitB12组高，对照组与VitB12组间差异无显著性。而cPLA2则和对照组与DEX组间在AnnexinⅠ和cPLA2测量差异无显著性。结论 AnnexinⅠ和cPLA2介导了糖皮质激素诱发腭裂的过程。VitB12未能阻遇DEX上调AnnexinⅠ的表达。但可以对抗DEX抑制cPLA2的作用，这可能是VitB12拮抗糖皮质激素致畸作用的机制之一。

Study on the expression level of Annexin Ⅰ、 cPLA2 and PCNA in cleft-palate mice induced by dexamethasone

OBJECTIVE: To test the changing expression level of Annexin I, cPLA(2) and PCNA in the palatine process of cleft-palate mice A/J and C57B/6j induced by dexamethasone. To discuss the developing mechanism of cleft-palate and the corresponding preventive methods. METHOD: s Pregnant mice A/J and C57BL/6j were randomly divided into normal group as blank control, group with deformity induced by dexamethasone, group given VitB(12) as antagonist to deforming factor, group given only VitB(12). The relative quantity of Annexin I, Cpla2 and PCNA were detected by immunoblotting. RESULTS: Among mice A/J, with the development of palatine process, Annexin I's expression level was increased in the normal group, and other groups showed the similar changes. Annexin I's expression level was significantly higher in group DEX and group DEX + VitB(12) than in normal group and VitB(12) group of, while there was no significant difference between normal group and VitB(12) group. But the changes of cPLA(2) and PCNA expression level was in an opposite direction, with development it decreased in the normal mice's palatine process. In mice C57B/6j there was no significant difference between normal group and group DEX on the measured quantity of Annexin I, cPLA(2) and CONCLUSIONS: Annexin I and cPLA(2) introduce glucocorticoid to induce cleft-palate. VitB(12) can not inhibit DEX's enhancing effect on the expression level of Annexin I, but it can antagonize DEX's inhibiting effect on expression level of cPLA(2), which is probably one of the mechanisms why VitB(12) antagonize glucocorticoid's deforming effect.