|
Objective: cleft palate (cleft of palate) is a common congenital malformation accounted for the vast majority in the craniofacial anomalies. It occurred to the lives of patients and their families and psychological greater impact. Currently, there are scholars on cleft palate mechanism to make the more basic and clinical research, and has made certain achievements. But it is a polygenic disease, its pathogenesis is still unclear. Cleft palate pathogenesis studies can provide broad prospects for the prevention and prenatal diagnosis of cleft palate. Retinoic acid (retinoic acid, RA) in the organism of the embryo development and organ formation, cell differentiation, and plays an important role in the maintenance of normal physiological homeostasis. During embryonic development, endogenous retinoic acid is closely related to the normal growth and development. Excess retinoic acid have significant side effects, and allows the expression of genetic errors leading to abnormal development of the embryo, induced the formation of tissues and organs malformations. Of retinoic acid signaling function is ultimately achieved through the regulation of gene transcription, such as growth factors, cytokines and their receptors, hormones, transcription factors, kinases and phosphatases, intracellular enzymes and effectors are regulated by retinoic acid . Foreign scholars in recent years, the regulation of gene expression of retinoic acid (retinoic acid, RA) and its relationship induced formation of cleft palate were studied, but it the RA induced cleft palate mechanism is still not clear. Transforming growth factor-β superfamily (transforming growth factorβ, TGFβ) are a class having a variety of biological activity of cytokines, in various aspects involved in embryonic development, its different types of cells can promote their proliferation, growth and differentiation, can also be The inhibition of cell growth, is bidirectional adjustment of a cell growth factor. Recently, scholars by first extracting a sample of the DNA, select specific genes labeled primers for PCR amplification, and then detecting the PCR amplification product. Screened TGFβ may cleft palate susceptibility gene. Therefore, the experimental pre-through retinoic acid C57BL/6J the Department mice cleft palate model on this basis by immunohistochemistry to detect the temporal and spatial variation of TGFβ1 and TGFβ3 expression in retinoic acid-induced cleft palate and normal C57BL/6J strain mice palate for further research to prepare. Methods: 10-week-old male weighing more than 25 grams, female C57BL/6J mice weighing more than 20 grams. 5:00 on the first evening of the male and female ratio of 2:1 in the same cage, the next day to check in as early as 8:00 vaginal plug the positive recorded as 0 days of gestation (the gestation 0day GD0). Total was pregnant rats (10) only obtained pregnant rats were randomly divided into two groups: the first group, the experimental group, a total of (5); second control group for the group, a total of (5). The experimental group pregnant rats at GD10 10:00 0.01ml / g body weight infusion 10mg/ml of retinoic acid vegetable oil solution, the control mice 0.01ml / g body weight perfusion vegetable oil. Experimental and control groups, respectively, in the GD14, GD15, GD16 3 time points experimental mice were sacrificed to remove the embryos. Take embryonic mouse head fixed, embedded after slicing, immunohistochemical detection of TGFβ1 and TGFβ3 expression of the palate in mice at various time points. Thus, the derived TGFβ1 and TGFβ3 expression induced by retinoic acid in the palatal cleft palate in mice and normal mice. Results: 1 retinoic acid treatment group and control group, the expression of mesenchymal TGFβ3 With the development of embryos has decreased, mesenchymal TGFβ3 expression GD14, GD16 retinoic acid treatment group and control group, GD15 to the TGFβ3 the expression of the drug group high side; early treatment group and the control group (GD14, GD15) of TGFβ1 expression is more consistent with the development of embryos was increased, however, in later stages (GD16) in the experimental group palate of TGFβ1 sudden expression of high compared with the control group. Crest epithelium TGFβ3 2 retinoic acid administration group (s) has been in a state of high expression in the control group crest epithelium TGFβ3 the expression gradually decreased with the development of the embryo; administration group crest epithelium TGFβ1 expression obvious with the development of embryos increased TGFβ1 expression crest epithelium in the control group increased first and then decreased. Retinoic acid administered group with the control group nasal side TGFβ3 expression in epithelial same GD14, GD15 dose group than the control group, GD16 control group slightly higher; TGFβ1 in the nasal side of the epithelium of the retinoic acid treatment group and the control group expression in GD14, GD15 low dose group than in the control group and the the GD16 experimental group TGFβ1 expression was significantly lower than the control group. Conclusion: 1, the experimental group TGFβ3 mesenchymal high quality of expression in early development (GD14, GD15) of TGFβ1 expression is low, TGFβ1 and TGFβ3 possibly through inhibition of mesenchymal cell proliferation, affecting palatal elevation , induced cleft palate. 2, the experimental group crest epithelial TGFβ3 always in high levels of expression may cause abnormal differentiation of the epithelial ridge to the oral side epithelium; late (GD16) TGFβ1 is expressed at high levels, may also promote the ridge epithelial abnormal differentiation. Can speculate TGFβ1 and TGFβ3 may induce abnormal differentiation of crest epithelial-induced cleft palate. 3, GD15, the nasal side of the experimental group epithelial TGFβ3 expression of the high side of TGFβ1 expression was decreased, the nasal side epithelium may induce abnormal differentiation. Can speculate TGFβ1 and TGFβ3 may cause abnormal differentiation of the nasal side of the epithelium, and can not be in contact with the nasal septum fusion induced cleft palate.
|