老年性骨质疏松症动物模型及其发病机制的研究进展  

Research progress of animal models and the pathogenic mechanism of senile osteoporosis

作　　者：李晓敏[1] 张岩[1] 

机构地区：[1]上海理工大学系统生物医学研究中心,上海200093

出　　处：《中国骨质疏松杂志》2015年第2期245-248,共4页Chinese Journal of Osteoporosis

基　　金：上海市教委科研创新重点项目(11ZZ137)

摘　　要：老年性骨质疏松症(SOP)是生物衰老在骨骼方面的一种特殊表现,对老年人的健康和生活质量造成了严重的威胁。随着人口老龄化的加快,如何防治SOP及其引发的骨折不仅成为了医学界急需解决的问题,也是一个社会化问题。建立合适的SOP动物模型能更好地指导其发病机理的探究,并为新药的研发提供帮助。本文主要总结了近几年来应用较多的3种SOP动物模型,包括SAMP6快速老化SOP动物模型、D-半乳糖致衰老性SOP动物模型、自然衰老性SOP动物模型,并对以上动物模型各自的发病机制进行综述。The special appearance of biological ageing in skeletal system is senile osteoporosis（SOP）,which impairs seriously the healthy state and life quality of the elderly.With the acceleration of population aging,how to prevent and treat SOP and SOPinduced osteoporotic fracture is a problem to be solved urgently in medical field,and is also a social problem.The development of appropriate animal models for SOP can benefit to explore the pathogenesis of SOP and to help the research and development of novel drugs.This review summarizes 3 SOP animal models,including the senescence-accelerated mouse strain P6,the D-galactoseinduced aging animal model,and the naturally aged animal model,which are more often used in recent years,and reviews the respective pathogenesis of each animal model.

关 键 词：老年性骨质疏松 动物模型 机制 

分 类 号：R681[医药卫生—骨科学]