期刊文献+

地塞米松对胎盘细胞生长及葡萄糖转运功能的影响

Effect of dexamethasone on placental cell growth and glucose transport function
原文传递
导出
摘要 目的探讨地塞米松(DEX)对胎盘细胞生长及葡萄糖转运功能的影响。方法孕32~34周的先兆早产孕妇160例,随机均分为DEX组和对照组。DEX组肌肉注射DEX 6mg,每12小时1次,持续2d;对照组不用DEX。两组孕妇分娩后各取10例胎盘组织样本,采用苏木素-伊红(HE)染色和TUNEL染色分别检测两组胎盘组织细胞核周长和细胞凋亡情况,qRT-PCR及Western blot检测两组糖皮质激素受体(GR)α、葡萄糖转运蛋白(GLUT)1和GLUT3的mRNA及蛋白表达。结果与对照组比较,DEX组的细胞核周长较长(P<0.01),细胞凋亡增多(P<0.05)。DEX组GRα、GLUT1和GLUT3 mRNA和蛋白表达较对照组减少(P<0.01或P<0.05)。结论DEX能够抑制胎盘细胞的生长,降低胎盘对葡萄糖的转运效率。 Objective To investigate the effect of dexamethasone (DEX) on placental cell growth and glucose transport function. Methods A total of 160 women of 32-34 weeks pregnancy with threatened premature labor was randomly and equally divided into two groups. Group D was given DEX 6 mg by intramuscular injection every 12 hours for two days. Group C was not given DEX treatment. Ten placenta samples were randomly selected from two groups after delivery, respectively. The circumference of nuclear and cell apoptosis were detected by HE staining and TUNEL staining in two groups, qRT-PCR and Western blot were used to detect the mRNA and protein expressions of glucocorticoid receptors(GR) a, glucose transporter(GLUT) 1 and GLUT3. Resets Compared to group C,group D had longer circumference of nuclear and more cell apoptosis(P〈0. 01 or P〈0. 05). The mRNA and protein expressions of GRa, GLUT1 and GLUT3 were decreased in group D than those in group C(P〈0. 01 or P〈0. 05). Conclusion DEX can inhibit the growth of placental cells and decrease the transport efficiency of glucose.
出处 《江苏医药》 CAS 2017年第20期1437-1440,F0002,共5页 Jiangsu Medical Journal
基金 浙江省自然科学基金(LQ15H040002) 杭州市科学发展计划项目(20140733Q06)
关键词 地塞米松 胎盘 葡萄糖转运 Dexamethasone Placenta Glucose transport
  • 相关文献

参考文献3

二级参考文献43

  • 1魏克伦,杨于嘉,姚裕家,杜立中,王庆红.中国住院新生儿流行病学调查[J].中国当代儿科杂志,2009,11(1):15-20. 被引量:211
  • 2朱小明.胎膜早破应用地塞米松是否诱发早产的观察[J].南通医学院学报,1994,14(1):77-78. 被引量:2
  • 3Rovers MM,Schilder AG,Zielhuis GA,Rosenfeld RM,张江平,杨妙丽,张全安.中耳炎[J].国外医学(耳鼻咽喉科学分册),2005,29(3):141-143. 被引量:435
  • 4Buttgereit F,Straub RH,Wehling M.Glucocorticoids in thetreat ment of rheumatic diseases:an update onthe mechanismsof action. Arthritis and Rheumatism . 2004
  • 5Giannoulias D,Haluska GJ,Gravett MG.Localization ofprostaglandin H synthase,prostaglandin dehydrogenase,corticotropin releasing hormone and glucocorticoid receptor inrhesus monkey fetal membranes with labor and in the pres-ence of infection. Placenta . 2005
  • 6Robert S,Franklin W,Richard N.A comparision of thebioavailability of oral and intramuscular dexamethasone inwomenin late pregnancy. Obstetrics and Gynecology . 1997
  • 7Challis J R G.Mechanism of parturition and preterm labor. Obstetrical and Gynecological Survey . 2000
  • 8Schwartz LB.Understanding human parturition. The Lancet . 1997
  • 9Elliott JP,Radin T.The effect of corticosteroid administra-tion on uterine activity and preterm labor in high-ordermultiple gestations. Obstetrics and Gynecology . 1995
  • 10Nikolai Petrovsky,Luis Socha,Diego Silva.Macrophage migration in-hibitory factor exhibits a pronounced circadian rhythm relevant to itsrole as a glucocorticoid counter-regulator. Immunology and CellBiology . 2003

共引文献10

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部