中国组织工程研究

中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (50): 9354-.doi: 10.3969/j.issn.1673-8225.2010.50.011

• 组织构建实验造模 • 上一篇    下一篇

胎儿生长受限SD大鼠模型的建立和相关信号转导机制

樊杨，贾咏存，纳文霞   

  1. 宁夏自治区人民医院妇产科，宁夏回族自治区银川市 750021
     
  • 出版日期:2010-12-10 发布日期:2010-12-10
  • 作者简介:樊杨☆，女，1970年生，宁夏回族自治区银川市人，汉族，2007年解放军第四军医大学毕业，博士，主任医师，主要从事妇科肿瘤及围产医学研究。 yangf0803@126.com
  • 基金资助:

    宁夏自然科学基金项目(编号：NZ09143)，项目名称：胎儿宫内生长受限的胰岛素抵抗及其MAPkinase信号转导机制。

Establishment of SD fetal growth restriction models and relative signal transduction mechanism

Fan Yang, Jia Yong-cun, Na Wen-xia   

  1. Department of Obstetrics and Gynecology, People’s Hospital of Ningxia Hui Autonomous Region, Yinchuan  750021, Ningxia Hui Autonomous Region, China
  • Online:2010-12-10 Published:2010-12-10
  • About author:Fan Yang☆, Doctor, Chief physician, Department of Obstetrics and Gynecology, People’s Hospital of Ningxia Hui Autonomous Region, Yinchuan 750021, Ningxia Hui Autonomous Region, China yangf0803@126.com
  • Supported by:

    the Natural Science Foundation of Ningxia Hui Autonomous Region, No. NZ09143*

PDF

400

摘要：

背景：研究发现，胎儿生长受限可造成胎儿代谢的适应性改变及多种内分泌激素系统重整，导致胎儿生长发育迟缓以及成年后胰岛素抵抗的发生。但胎儿生长受限演变为胰岛素抵抗的分子机制尚不明确。
目的：探讨胎儿宫内生长受限发生胰岛素抵抗的潜在分子机制，为早期诊断和临床干预成年后代谢性疾病提供理论依据。
方法：SD大鼠分成胎儿生长受限仔鼠组和正常对照仔鼠组。胎儿生长受限仔鼠组大鼠构建胎儿生长受限SD大鼠动物模型。提取各组仔鼠胎盘组织蛋白质，应用特异性抗磷酸化抗体进行免疫共沉淀和Western blot方法对有丝分裂素激活蛋白激酶信号途径上各蛋白激酶及其抑制剂的活性进行分析。
结果与结论：在胎儿生长受限仔鼠组中，有丝分裂素激活蛋白激酶信号转导途径中细胞外信号调节激酶1/2、应激活化蛋白激酶/c-Jun氨基末端激酶及Raf-1蛋白激酶活性比正常对照组显著降低(P < 0.05)，p38有丝分裂素激活蛋白激酶活性两组比较差异无显著性意义(P > 0.05)；相反，有丝分裂素激活蛋白激酶信号转导途径中各抑制剂在胎儿生长受限仔鼠组中表达水平较正常对照组中表达显著升高(P < 0.05)。结果表明，胎儿生长受限的发生与有丝分裂素激活蛋白激酶及细胞凋亡信号传导机制异常密切相关。

关键词: 胎儿, 生长受限, 胰岛素抵抗, 有丝分裂素激活蛋白激酶, 有丝分裂素激活蛋白激酶信号转导途径, 细胞凋亡

Abstract:

BACKGROUND: Studies found that fetal growth restriction can lead to adaptive change of metabolism and redintegration of hormones system, result in child development delay and insulin resistance after grow up. However, the molecule mechanism of the variation during pathological process from fetal growth restriction to insulin resistance remains poorly understood. 
OBJECTIVE: To explore the potential molecule mechanism of fetal growth restriction to insulin resistance, and to provide basis for the early diagnosis and intervention on metabolic disease.
METHODS: SD rats were randomly divided into the fetal growth restriction group and normal control group. Rats in the former group were prepared for fetal growth restriction models. The placenta protein was extracted from each group, and the protein kinase activity and inhibitor on MAP kinase (MAPK) signaling pathway were analyzed by plication of specific anti-phosphorylation antibody immunoprecipitation and Western blot.
RESULTS AND CONCLUSION: MAPK signal transduction pathway of ERK1/2, SAPK/JNK and Raf-1 protein kinase activity of the fetal growth restriction group were obviously decreased than those of the normal control group (P < 0.05), but the p38MAPK, MAP Kinase Kinases protein kinase activity in two groups did not change significantly (P > 0.05). In contrast, MAPK signal transduction pathway inhibitors in the fetal growth restriction group were higher than that of the normal control group (P < 0.05). The incidence of fetal growth restriction is closely related to abnormal MAP kinase signal transduction and apoptosis mechanism.

中图分类号: