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维生素 B12 对 2,3,7,8-四氯二苯并对二恶英和地塞米松诱导的小鼠腭裂的影响。

Effect of vitamin B12 on cleft palate induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin and dexamethasone in mice.

机构信息

State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China; Department of Cleft Lip and Palate Surgery, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China; Department of Biochemistry & Molecular Biology, University of North Dakota School of Medicine & Health Sciences, Grand Forks, ND 58203, USA.

出版信息

J Zhejiang Univ Sci B. 2014 Mar;15(3):289-94. doi: 10.1631/jzus.B1300083.

DOI:10.1631/jzus.B1300083
PMID:24599693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3955916/
Abstract

The purpose of this study was to investigate the effect of vitamin B12 on palatal development by co-administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and dexamethasone (DEX). We examined the morphological and histological features of the palatal shelf and expression levels of key signaling molecules (transforming growth factor-β3 (TGF-β3) and TGF-β type I receptor (activin receptor-like kinase 5, ALK5)) during palatogenesis among a control group (Group A), TCDD+DEX exposed group (Group B), and TCDD+DEX+vitamin B12 exposed group (Group C). While we failed to find that vitamin B12 decreased the incidence of cleft palate induced by TCDD+DEX treatment, the expression levels of key signaling molecules (TGF-β3 and ALK5) during palatogenesis were significantly modulated. In TCDD+DEX exposed and TCDD+DEX+vitamin B12 exposed groups, palatal shelves could not contact in the midline due to their small sizes. Our results suggest that vitamin B12 may inhibit the expression of some cleft palate inducers such as TGF-β3 and ALK5 in DEX+TCDD exposed mice, which may be beneficial against palatogenesis to some degree, even though we were unable to observe a protective role of vitamin B12 in morphological and histological alterations of palatal shelves induced by DEX and TCDD.

摘要

本研究旨在通过联合给予 2,3,7,8-四氯二苯并对二恶英(TCDD)和地塞米松(DEX)来研究维生素 B12 对腭发育的影响。我们检查了对照组(A 组)、TCDD+DEX 暴露组(B 组)和 TCDD+DEX+维生素 B12 暴露组(C 组)在腭发生过程中腭突的形态和组织学特征,以及关键信号分子(转化生长因子-β3(TGF-β3)和 TGF-β 型 I 受体(激活素受体样激酶 5,ALK5))的表达水平。虽然我们未能发现维生素 B12 降低了 TCDD+DEX 处理引起的腭裂发生率,但关键信号分子(TGF-β3 和 ALK5)在腭发生过程中的表达水平明显受到调节。在 TCDD+DEX 暴露和 TCDD+DEX+维生素 B12 暴露组中,由于腭突较小,无法在中线接触。我们的结果表明,维生素 B12 可能抑制 DEX+TCDD 暴露小鼠中某些腭裂诱导物如 TGF-β3 和 ALK5 的表达,这可能在某种程度上有益于腭发生,尽管我们未能观察到维生素 B12 在 DEX 和 TCDD 诱导的腭突形态和组织学改变中具有保护作用。

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本文引用的文献

1
[The preliminary study on transforming growth factor-beta 3, activin receptor-like kinase 5 expression in 2, 3, 7, 8-tetrachloro-p-dibenzodioxin and dexamethasone induced palatal cleft in mice].[转化生长因子-β3、激活素受体样激酶5在2,3,7,8-四氯对二苯并二恶英和地塞米松诱导的小鼠腭裂中表达的初步研究]
Hua Xi Kou Qiang Yi Xue Za Zhi. 2010 Aug;28(4):356-60.
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Analyzing real-time PCR data by the comparative C(T) method.通过比较Ct法分析实时荧光定量PCR数据。
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A preliminary study on the teratogenesis of dexamethasone and the preventive effect of vitamin B12 on murine embryonic palatal shelf fusion in vitro.地塞米松致畸作用及维生素B12对体外培养小鼠胚胎腭突融合预防作用的初步研究
J Zhejiang Univ Sci B. 2008 Apr;9(4):306-12. doi: 10.1631/jzus.B0710625.
4
Epithelial and ectomesenchymal role of the type I TGF-beta receptor ALK5 during facial morphogenesis and palatal fusion.I型转化生长因子-β受体ALK5在面部形态发生和腭融合过程中的上皮和外胚间充质作用。
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Transforming growth factor-beta3 restores fusion in palatal shelves exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin.转化生长因子-β3可恢复暴露于2,3,7,8-四氯二苯并对二恶英的腭突的融合。
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Overexpression of Smad2 in Tgf-beta3-null mutant mice rescues cleft palate.在Tgf-beta3基因缺失的突变小鼠中,Smad2的过表达挽救了腭裂。
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