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张明敏,程亮亮,董莉萍.补肾安胎方对胚泡着床障碍模型小鼠着床局部PGI2及其核受体的影响[J].中国中西医结合杂志,2008,(3):228-232
补肾安胎方对胚泡着床障碍模型小鼠着床局部PGI2及其核受体的影响
Effect of Bushen Antai Recipe on Prostaglandin 12 Expression and Its Nuclear Receptor at Implantation Site in Mice with Blastocyst Implantation Dysfunction
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DOI:
中文关键词:  补肾安胎方  着床  前列环素I2  核受体过氧化物酶体增殖激活因子受体δ
英文关键词:Bushen Antai Recipe  implantation  prostaglandin I2  peroxisome proliferators-activated receptor
基金项目:国家自然科学基金(No.30371829)
作者单位
张明敏 华中科技大学同济医学院附属同济医院中西医结合科 
程亮亮 华中科技大学同济医学院附属同济医院中西医结合科 
董莉萍 华中科技大学同济医学院附属同济医院中西医结合科 
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中文摘要:
      目的观察补肾安胎方对胚泡着床障碍小鼠着床局部前列环素I2(PGI2)及其核受体过氧化物酶体增殖激活因子受体δ(PPARδ)表达的影响。方法将妊娠小鼠随机分为正常组、模型组和中药组(每天灌服补肾安胎液12.4 g/kg),在妊娠第4、5、6、8天取3组小鼠妊娠子宫,采用放射免疫法测定PGI2含量,RT-PCR和免疫组织化学方法检测PPARδmRNA及蛋白的表达。结果模型组小鼠子宫内膜着床点PCI2含量明显低于正常组(P<0.01),而中药组PGI,含量较模型组显著增高(P<0.01)。模型组小鼠子宫内膜中PPARδ的表达均滞后于正常组(P<0.05);小鼠子宫内膜中PGI2含量和PPARδ的表达正常组和中药组组间比较,差异无统计学意义。结论补肾安胎方可能通过促进胚泡着床局部的PGI2及其核受体PPARδ的表达来改善胚泡着床障碍小鼠的胚泡着床。
英文摘要:
      Objective To observe the effect of Bushen Antai Recipe(BAR)on expression of prostaglandin I2 (PGI2)and its nuclear receptor peroxisome proliferators-activated receptorδ(PPARδ)at implantation site in mice with blastocyst implantation dysfunction.Methods Pregnant mice were divided into three groups randomly,the normal group,the model group and the BAR group.The pregnant uterus of all mice was cut off on the 4th(D4), 5th(D5),6th(D6)and 8th(D8)day of pregnancy for determining the PGI2 expression with radio immunoassay; and the mRNA and protein expression of PPARδwith RT-PCR and immunohistochemistry at implantation site.Re- suits PGI2 expression in the model group was obviously lower than that in the normal group(P<O.01),and also lower than that in the BAR group(P<0.01),while the index was insignificantly different between the normal and the BAR group.Compared with the normal group,the expression of PPARδin the model group was delayed tempo- rally and spatially(P<0.05),while that in the BAR group was not significantly different.Conclusion BAR can improve the implantation in mice with blastocyst implantation dysfunction through promoting the PGI2 expression and its nuclear receptor PPARδat implantation site.
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