文章摘要
郭 健,苗登顺.PTH缺乏经细胞外钙介导卵巢血管生成障碍而致生殖能力降低[J].南京医科大学学报,2009,29(5):628~633
PTH缺乏经细胞外钙介导卵巢血管生成障碍而致生殖能力降低
Parathyroid hormone deficiency resulted in fertility defects mediated through extracellular calcium
投稿时间:2008-12-22  
DOI:10.7655
中文关键词: PTH  基因敲除  不孕  饮食钙  血管发生
英文关键词: PTH  gene knock-out  infertility  calcium diet  angiogenesis
基金项目:
作者单位
郭 健 南京医科大学人体解剖学系,江苏 南京 210029 
苗登顺  
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中文摘要:
      目的:探讨甲状旁腺素(PTH)缺乏引起生殖功能降低的机制?方法:使用组织学,免疫组织化学和Western blot的方法比较分析了同窝4个月PTH基因敲除纯合子小鼠和野生型小鼠分别给予正常钙(1%)?低钙(0.01%)及高钙饮食(2%)后生殖能力?卵巢成熟卵泡数量?黄体形成及血管生成的差异?结果:与同窝野生型雌性小鼠(PTH+/+)相比,正常饮食PTH基因敲除纯合子小鼠(PTH-/-)生殖能力下降,成熟卵泡数量及黄体生成减少,卵巢血管发生减少;低钙饮食PTH-/-表现为完全不孕,成熟卵泡数量进一步减少和黄体缺失,卵巢血管发生减少更为明显;而高钙饮食PTH-/-生殖能力?成熟卵泡数量?黄体形成及血管发生均恢复正常?结论:PTH缺乏经细胞外钙介导卵巢血管生成障碍而致生殖能力降低?
英文摘要:
      Objective:To investigate the mechanism of the PTH deficiency resulting in fertility defects in female mice. Methods:Capacity of fertility,the number of tertiary follicles,corpus luteum formation and angiogenesis were compared between PTH knock-out and wild-type littermates at 4 months of ages fed either on normal calcium(1%),low calcium(0.01%) and high calcium(2%) diet by using histology,immunohistochemistry and Western-blot,respectively. Results:Compared with wild-type mice,on the normal calcium diet,PTH knock-out mice displayed lower fertility capacity,decreased number of tertiary follicles and formation of corpus luetum and reduced the angiogenesis in ovary; On the low calcium diet,PTH knock-out mice displayed completely infertile,further decreased number of tertiary follicles without the corpus luteum formation and reduced angiogenesis in ovary more dramatically; Whereas on the high calcium diet,PTH knock-out mice were normalized for all fertility parameters including the number of tertiary follicles,the corpus luteum formation and angiogenesis in ovary. Conclusion:PTH deficiency resulted in fertility defects mediated through extracellular calcium.
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