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| 雌激素与尾悬吊法导致雄性C57小鼠骨质疏松关系的研究 |
| The study on the relationship between estrogen and tail-suspension-induced osteoporosis in male C57 mice |
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| DOI：10.3969/j.issn.1006-7108.2017.01.002 |
| 中文关键词: 骨质疏松 尾悬吊 骨参数 NMDA受体 |
| 英文关键词:Osteoporosis Tail-suspension Bone parameters NMDA receptor |
| 基金项目:江苏省六大人才高峰资助（2013-WSN-091）；江苏省临床科技项目基金（BL2012002） |
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| 中文摘要: |
| 目的 探讨雌激素对尾悬吊导致雄性C57小鼠骨质疏松的影响及其内在机制。 方法 32只成年C57BL/6J雄性小鼠，随机分成4组：对照组（control，C），模型组(model，M)，雌激素组(estrogen，E)，雌激素+雌激素受体抑制组(estrogen+ICI 182,780，E+I)。除C组外其余组小鼠尾悬吊两周，所有小鼠在第15d处死，取小鼠血清进行生化指标分析，取小鼠右侧股骨进行显微CT扫描和形态学染色，取小鼠左侧股骨进行生物力学检测并取股骨远端研磨后进行蛋白检测。 结果 尾悬吊两周导致雄性C57小鼠股骨出现明显骨质疏松，M组与C组相比差异有显著的统计学意义（P<0.05）。雌激素干预能抑制骨质流失，E组多数骨相关参数与对照组相比，差异无统计学意义（P>0.05）。而使用雌激素受体拮抗剂ICI182,780之后，雌激素骨保护效应消失，与M组相比差异无统计学意义（P>0.05）。尾悬吊两周导致股骨远端离子型谷氨酸受体NMDA亚型NR2A表达降低，雌激素升高骨组织中NR2A表达水平。 结论 雄性C57小鼠尾悬吊2w表现出显著骨质疏松，雌激素通过激活雌激素受体明显改善骨质流失，可能是通过促进骨组织中NR2A表达而实现成骨细胞增殖和分化。 |
| 英文摘要: |
| Objective To explore the effect and underlying mechanism of estrogen on male mouse osteoporosis induced by tail-suspension (TS). Methods Thirty-two male C57BL/6J mice were randomly divided into 4 groups: control (C) group, model (M) group, estrogen (E) group, and estrogen+ICI182,780 group (E+I). All mice received TS for 2 weeks apart from the C group. Mice were then sacrificed in 15 days and the serum and right femurs were collected for biochemical test, micro-CT scanning, and morphological observation. The left femurs were collected for biomechanical test and Western blotting analysis. Results The M group showed obvious bone loss after TS and had significant difference compared with the C group (P<0.05). Application of exogenous estrogen effectively inhibited bone turnover and conserve bone mass, and most of bone-associated parameters in the E group showed no difference with the C group (P>0.05). The protective effect of estrogen disappeared when the mice were treated with ICI182,780, and most of parameters in the E+I group showed no difference compared with those in the M group (P>0.05). The expression of N-methyl-D-aspartic acid (NMDA) receptor subunit NR2A decreased in TS mice in 2 weeks, while estrogen improved the level of NR2A in bone tissue. Conclusion Significant bone loss appears in mice in TS-treated group. Estrogen improves bone mass by binding with the estrogen receptors. The estrogenic effect of bone protection might be induced by elevating the expression of NMDA receptor subunit NR2A, and then by promoting osteoblast proliferation and differentiation. |
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