期刊文献+

逍遥丸对小鼠卵母细胞分泌因子生长分化因子-9受体及Smads通路的影响 被引量:1

Effects of Xiaoyao Pill on mouse oocyte-secreted factors GDF-9 receptors and Smads signal pathway
原文传递
导出
摘要 目的:观察逍遥丸对小鼠卵母细胞分泌因子生长分化因子-9(GDF-9)受体BMPRⅡ、ALK-5及下游Smads通路中Smad2、Smad3的影响。方法:将120只小鼠随机分为4组:疏肝高、低剂量组;COH组和空白对照组,每组30只。应用免疫组化和实时荧光定量PCR(Real-time PCR)法分别测定卵母细胞中BMPRⅡ、ALK-5、Smad2、Smad3蛋白及mRNA的表达。结果:与空白对照组比较,COH组及疏肝低剂量组BMPRⅡ蛋白及mRNA表达无统计学意义;疏肝高剂量组BMPRⅡ蛋白及mRNA表达增强(P<0.05)。ALK-5、Smad2、Smad3蛋白及mRNA表达在各组间比较均无统计学意义。结论:高剂量逍遥丸可上调卵母细胞中GDF-9Ⅱ型受体BMPRⅡ蛋白及mRNA表达,但并未影响ALK-5、Smad2、Smad3的表达,提示逍遥丸影响卵子质量的机制与GDF-9一型受体及下游Smads通路无关。 Objective: To investigate the effects of Xiaoyao Pill on the expressions of BMPR I and ALK-5,that oocytesecreted factors GDF-9 receptors,and the expressions of Smad2 and Smad3 in Smads Signal Pathway.Methods:120 mice were randomly divided into 4 groups: Shugan high,low dose groups,COH group and control group,with 30 mice in each group.The protein and mRNA expressions of BMPR I,ALK-5,Smad2 and Smad3 in mouse oocytes were detected by immunohistochemistry and Real-time PCR,respectively.Results: The protein and mRNA expressions of BMPR I in COH group and Shugan low dose group were both no statistical significance compared with those in blank control group.The protein and mRNA expressions of BMPR I in Shugan high dose group were higher than those in blank control group(P〈0.05).There was no statistical significance in the protein and mRNA expressions of ALK-5,Smad2 and Smad3 among each group(P〈0.05).Conclusion: The high dose Xiaoyao Pill can up-regulate the protein and mRNA expression of BMPR I in oocytes.But it can not influence the expressions of ALK-5,Smad2 and Smad3.The mechanism that Xiaoyao Pill influenced the quality of oocytes may be related to GDF-9 receptor rather than Smads signal pathway.
出处 《中华中医药杂志》 CAS CSCD 北大核心 2015年第4期1076-1078,共3页 China Journal of Traditional Chinese Medicine and Pharmacy
基金 国家自然科学基金项目(No.81173294)~~
关键词 逍遥丸 卵母细胞 生长分化因子-9 成骨蛋白受体2型 ALK-5 SMAD2 Smad3 Xiaoyao Pill Oocyte GDF-9 BMPR I ALK-5 Smad2 Smad3
  • 相关文献

参考文献18

二级参考文献64

共引文献80

同被引文献12

引证文献1

二级引证文献1

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