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作 者:张雪竹[1] 于建春[1] 刘存志[1] 彭应梅[1] 韩景献[1]
机构地区:[1]天津中医药大学第一附属医院针灸研究所,300193
出 处:《国际内分泌代谢杂志》2006年第4期245-247,共3页International Journal of Endocrinology and Metabolism
基 金:天津市卫生局资助课题(2005034)
摘 要:骨质疏松发病率较高,发病机制复杂,尚需开展广泛深入的相关研究。但目前诱发的骨质疏松模型均只侧重表现其发病的某一环节,应用上有局限。快速骨老化模型小鼠SAMP6(senescenceaccelerated mouse prone 6)更好地再现了老年性骨质疏松的病理变化,如低骨密度、低峰值骨量、骨微观结构退化等,是研究骨质疏松发病机理及开发有效治疗手段的理想模型。Osteoporosis is a progressive bone disease with a high incidence. The pathogenesis of osteoporosis is still unknown, so it is necessary to study the pathogenic mechanisms of osteoporosis extensively and deeply. Many animal models for osteoporosis only concentrate on one facet of the disease and can not be used widely. Compared with other models for osteoporosis, the biological characteristics of bone in senescence-accelerated mouse prone 6 (SAMP6) are analogous to changes occurred in aging human skeleton, including low peak bone mass, low bone mineral density and uhrastructural changes of bone, so SAMP6 is a predominant and functionally relevant model in understanding the pathogenesis and developing effective therapeutics of senile osteoporosis.
关 键 词:骨质疏松 动物模型 快速老化小鼠SAMP6
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