去卵巢对硬骨素基因敲除小鼠骨密度及骨微结构的影响
The effect of ovariectomy on bone mineral density and bone microstructure of SOST gene knockout mice
摘要目的:观测硬骨素基因敲除(SOST -/-)小鼠在失去雌激素作用后骨密度和骨微结构的变化。 方法:12只4周龄SOST -/-小鼠,随机分2组( n=6):去卵巢组(SOV),假手术组(SSO);12只野生型小鼠随机分为2组( n=6):野生型去卵巢组(WTO),野生型假手术组(WTS)。12周后处死小鼠,腰椎行显微CT扫描分析。观察比较4组小鼠骨密度、骨小梁体积分数、骨小梁数量、骨小梁厚度。 结果:SOV与SSO组之间骨密度、骨小梁体积分数、骨小梁数量、骨小梁厚度差异无统计学意义( P>0.05),SOV和SSO组骨密度、骨小梁体积分数、骨小梁数量和骨小梁厚度均较WTO和WTS组显著增高,差异有统计学意义( P<0.001)。WTO组骨密度、骨小梁体积分数、骨小梁数量均较WTS组显著降低,差异有统计学意义( P=0.017、0.039、0.021);两组间骨小梁厚度差异无统计学意义( P=0.109)。 结论:硬骨素基因敲除小鼠表现为高骨量,去卵巢不会导致骨量丢失和骨微结构退变,提示硬骨素是潜在的绝经后骨质疏松治疗靶点。
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abstractsObjective:To observe the changes in bone mineral density and microstructure parameters in sclerostin (SOST) gene knockout (SOST -/-) mice after ovariectomy. Methods:Twelve 4-week-old SOST knockout mice were randomly divided into two groups ( n=6): ovariectomized group (SOV), sham operated group (SSO). Twelve wild-type mice were randomly divided into two groups ( n=6): wild-type ovariectomized group (WTO), wild-type sham operated group (WTS). Twelve weeks later, mice were sacrificed and one lumbar vertebra of each mouse was selected for micro-CT analysis. The bone mineral density, trabecular volume fraction, trabecular number and trabecular thickness were observed and compared in the 4 groups. Results:There was no difference in bone mineral density, trabecular volume fraction, trabecular number and trabecular thickness between SOV and SSO groups. Bone mineral density, trabecular volume fraction, trabecular number and trabecular thickness in SOV and SSO groups were significantly higher than those in WTO and WTS groups ( P<0.001). Bone mineral density, trabecular volume fraction and trabecular number in WTO group were significantly lower than those in WTS group ( P=0.017, 0.039, 0.021, respectively). There was no difference in trabecular thickness between WTO and WTS groups. Conclusions:Sclerostin knockout mice showed high bone mass, and ovariectomy did not lead to bone loss and bone microstructure degeneration, which indicates that slerostin is a potential therapeutic target for postmenopausal osteoporosis.
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