本文選題：Sox4 + 腭裂　； 參考：《山西醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:探討Sox4基因在BALB/c正常小鼠與腭裂模型腭突發(fā)育過程中的表達差異,初步研究該基因在小鼠上腭發(fā)育過程中的作用及其與腭裂發(fā)生的關(guān)系。方法:腭裂發(fā)生率統(tǒng)計:將12只BALB/c孕鼠平均分為兩組,將實驗組孕鼠于GD10(gestation day 10)一次性管飼50mg/kg維甲酸(retinoic acid,RA),對照組孕鼠給予管飼等量玉米油。在GD17上午8時將孕鼠處死,剖腹取得胎鼠,放大鏡下觀察每組胎鼠腭裂形成情況,統(tǒng)計腭裂發(fā)生率。Sox4蛋白檢測:按照上述方法獲取對照組及實驗組孕鼠各15只。分別在GD13、GD14、GD15上午8時處死實驗組與對照組孕鼠各5只,剖腹剪取胎鼠頭部標(biāo)本共253例,常規(guī)石蠟包埋及切片。利用HE染色觀察胎鼠腭突發(fā)育過程中的形態(tài)變化,采用免疫組織化學(xué)方法檢測目的蛋白在各組間不同時期腭突中的表達差異。結(jié)果:1.在統(tǒng)計腭裂發(fā)生率的實驗中對照組共獲得胎鼠55只,其中腭裂胎鼠為0只;實驗組共獲得胎鼠52只,腭裂胎鼠為44只。由此得出GD10給予50mg/kg維甲酸誘導(dǎo)BALB/c小鼠腭裂發(fā)生率為84.6%.可誘導(dǎo)穩(wěn)定的腭裂模型。2.獲得HE染色切片23例,結(jié)果顯示對照組雙側(cè)腭突在GD14發(fā)生水平向翻轉(zhuǎn)并接觸融合,實驗組腭突翻轉(zhuǎn)推遲至GD15但并未融合。3.免疫組化實驗共獲得切片219例,結(jié)果顯示,Sox4在實驗組與對照組腭突的被覆上皮及腭中線上皮中均有表達,用平均光密度值[1]分析對照組GD13-GD15組內(nèi)兩兩對比皆有差異(p0.05),且在GD14表達量最高。實驗組中GD13、GD14與GD15之間的表達對比均無差異(p0.05)。實驗組與對照組組間對比在GD13表達無差異(p0.05),GD14對照組高于實驗組(p0.05),GD15實驗組高于對照組(p0.05)。結(jié)論:Sox4在腭裂與正常腭突中GD14-GD15的表達存在明顯差異,在腭突融合期發(fā)揮調(diào)節(jié)作用。
[Abstract]:Objective: to investigate the difference of expression of Sox4 gene in the development of palatal process in normal BALB/c mice and cleft palate model, and to study the role of Sox4 gene in the development of upper palate in mice and its relationship with cleft palate. Methods: the incidence of cleft palate in 12 pregnant BALB/c rats was divided into two groups on average. The pregnant rats in the experimental group were given 50mg/kg retinoic acididate once, and the pregnant rats in the control group were given the same amount of corn oil. The pregnant mice were killed at 8: 00 am in GD17, and the fetal rats were obtained by laparotomy. The cleft palate was observed in each group under a magnifying glass, and the incidence rate of cleft palate. Sox4 protein was detected. According to the above methods, 15 pregnant rats in the control group and 15 in the experimental group were obtained. Five pregnant rats of the experimental group and the control group were killed at 8: 00 am of GD13, GD14 and GD15, and 253 fetal rat head specimens were taken by caesarean section. The specimens were embedded and sliced in paraffin. The morphological changes of palatine process in fetal rats were observed by HE staining and the expression of target protein in palatine process at different stages was detected by immunohistochemical method. The result is 1: 1. In the experiment of counting the incidence of cleft palate, 55 fetal rats were obtained in the control group, including 0 in the experimental group, 52 in the experimental group and 44 in the cleft palate fetus. The incidence of cleft palate in BALB/c mice induced by 50mg/kg retinoic acid by GD10 was 84. 6%. It can induce stable cleft palate model. He stained sections were obtained in 23 cases. The results showed that the bilateral palatine process in the control group was horizontally reversed and fused in contact with GD14, while the palatine process turnover in the experimental group was delayed to GD15 but did not fuse. 3. A total of 219 specimens were obtained by immunohistochemical method. The results showed that Sox4 was expressed in the coated epithelium and midline epithelium of palatine process in the experimental group and the control group. The average optical density value [1] was used to analyze the difference between two contrast groups in the GD13-GD15 group of the control group, and the highest expression of GD14 was found in the control group. There was no difference between the expression of GD13, GD14 and GD15 in the experimental group (p0.05). There was no difference in the expression of GD13 between the experimental group and the control group. The expression of GD14 in the control group was higher than that in the experimental group (p0.05) and that in the control group was higher than that in the control group (P 0.05). Conclusion the expression of GD14-GD15 in cleft palate is significantly different from that in normal palatine process, and it plays a regulatory role in palatine process fusion.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R782.2

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