中国骨质疏松杂志

地塞米松对护骨素基因敲除小鼠骨微结构的影响

The effect of dexamethasone on bone micro-architecture in OPG" " mice

DOI：10.3969/j.issn.1006.7108.2016.07.001

英文关键词:Dexamethasone Mouse Osteoprotegerin Gene knockout Micro-architecture Bone mineral density

基金项目:Dexamethasone ； Mouse ； Osteoprotegerin ； Gene knockout ； Micro-architecture ； Bone mineral density

作者	单位
段新云1 马育林1 旷小艳1 周培文1 袁妙兰1 盛志峰2*	1. 南方医科大学附属小榄医院，中山528415 2. 中南大学湘雅二医院代谢内分泌研究所，长沙410011

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中文摘要:

目的探讨小剂量地塞米松对生长期小鼠骨密度及骨微结构的影响及其与OPG途径的关系。方法 20只4周龄 OPG–/–雌性小鼠及20只野生型小鼠随机分四组（n = 10):野生型安慰剂组（WT + saline),野生型地塞米松干预组（WT + DEX，地塞米松lmg/kg体重，肌肉注射，每周3次）.OPG–/–敲除小鼠安慰剂组（OPG–/–+ saline) , OPG 敲除小鼠DEX干预组（OPG–/–+DEX,地塞米松1 mg/kg体重，肌肉注射，每周3次）。6周后处死小鼠，一侧胫骨行显微CT扫描分析。结果 OPG–/–组的组织骨密度、骨小梁体积分数、骨小梁数量、骨小梁厚度均较其他三组降低（P< 0.05)。OPG–/– + DEX组的组织骨密度、骨小梁体积分数、骨小梁数量、骨小梁厚度均较WT及WT + DEX组降低（P<0.05)。OPG–/–组的骨小梁模型因子及骨小梁分离度均较其他三组增加（P<0.05) ;OPG–/–+ DEX组的骨小梁模型因子及骨小梁分离度均较WT及WT + DEX组增加（P<0.05)。WT及WT +DEX组之间骨小梁微结构参数均无统计学差异。结论在生长期小鼠OPG基因功能缺失时，地塞米松有部分拮抗骨量丢失的作用，表明除了OPG/RANKL途径，地塞米松对骨代谢的影响是多途径的。

英文摘要:

Objective To observe the effect of low-dose dexamethasone on bone mineral density and micro-architecture in growing mice without OPG gene. Methods Twenty 4-week-old female OPG–/– mice and twenty 4-week-old wild type mice were randomly assigned to 4 groups (w = 10) ： wild type and placebo group (WT + saline)，wild type and dexamethasone group (WT + DXM, 1 mg/kg, intramuscular injection, 3 times/w) , OPG–/– and placebo group ( OPG–/– + saline) , and OPG–/– and dexamethasone group (OPG–/– + DEX, 1 mg/kg, intramuscular injection, 3 times/w). The mice were sacrificed after 6 weeks. One side of the tibia of each mouse was selected for micro-CT analysis. Results Tb. N, BS/BV, Tb. Th, and tBMD significantly decreased in OPG–/– mice than those in the other three groups ( P <0.05). Tb. N, BS/BV, Tb. Th, and tBMD significantly decreased in OPG–/– + DEX mice than those in WT and WT + DEX mice (P<0. 05). Tb. Pf and Tb. Sp significantly increased in OPG–/– mice than those in the other three groups (P<0.05). Tb. Pf and Tb. Sp significantly increased in OPG–/– + DEX mice than those in WT and WT + DXM mice (P < 0. 05). BMD and bone micro-architecture parameters were not significantly different between WT and WT + DXM mice. Conclusion Dexamethasone partly extenuates the bone loss in growing mice without OPG gene function. It indicates that in addition to OPG/RANKL pathway, dexamethasone affects bone metabolism through multiple pathways.

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