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作 者:顾怡然[1] 章蓉[1] 竺淑佳[1] 张冬丽[1] 陈逸群[1] 孙丽娟[1] 梅兵[1]
机构地区:[1]华东师范大学脑功能基因组学研究所,上海200062
出 处:《复旦学报(自然科学版)》2007年第6期874-877,共4页Journal of Fudan University:Natural Science
基 金:科技部"973计划"项目子课题资助项目(2003CB716602)
摘 要:研究了卵巢摘除致雌性大鼠骨质疏松过程中Klotho基因表达的变化,探讨雌激素缺失引起骨质疏松发生的可能分子机制.摘除卵巢并喂以特殊饲料致大鼠骨质疏松后,分别测定骨质疏松组和对照组大鼠血清中的钙浓度与碱性磷酸酶含量,X射线法检测两组大鼠股骨密度,实时荧光定量PCR评估两组大鼠肾脏组织中Klotho基因的表达量.结果显示,与对照组相比,卵巢摘除后大鼠血钙浓度降低,碱性磷酸酶含量升高,骨密度减少,同时肾脏组织中Klotho基因表达显著下调.提示Klotho基因的下调及其对相关信号传导通路的影响可能是雌激素缺失导致骨质疏松的分子机制之一.Osteoporosis is a complex disease which is known to be influenced by many nutritional, hormonal, environmental and genetic factors. To study molecular mechanisms of Osteoporosis induced by estrogen-deficient, we applied the ovariectomized rats as the animal model, measured their .serum calcium, alkaline phosphatase(ALP) and their bone mineral density(BMD), evaluated Klotho gene expression profile of kidney by real time quantitative PCR. The data show that estrogen-deficient decreased Ca^2 + concentration ( from 2. 633 ± 0. 030 2 mg/L. to 2. 441 ± 0. 033 6 mg/L.) and BMD ( from 0. 051 0 ± 0. 004 42 g/cm^2 to 0. 034 7 ± 0. 004 42 g/cm^2 ), increa,;ed ALP content ( from 323. 750 ± 22. 920 U/L. to 511. 778 ± 26. 272 U/L.), altered the expression level of Klotho gene significantly ( from 0. 098 9 ± 0. 004 43 to 0. 040 0 ± 0. 001 80), so resulting in Osteoporosis of rats. This result suggests that down-regulation of Klotho gene could be one of the molecular mechanisms underlying Osteoporosis induced by estrogen-deficient.
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