Nrf2的失活对应力负荷下的骨形成的影响  

Inactivation of Nrf2 Decreases Load-driven Bone Formation

作　　者：杨杨[1] 徐爱华[1] 戴奇[1] 张佳星[1] 孙永新[1] 

机构地区：[1]中国医科大学附属第一医院康复医学科,沈阳110001

出　　处：《中国医科大学学报》2015年第6期513-515,共3页Journal of China Medical University

基　　金：沈阳市科技技术计划项目(113882);辽宁省科学技术计划项目社会发展攻关计划项目(2010225034)

摘　　要：目的通过核转录因子2(Nrf2)基因敲除小鼠探索Nrf2在应力所致骨形成中的作用。方法通过PCR检测选取同窝杂交出生的小鼠Nrf2基因敲除(KO)组及野生(WT)组,按时给予尺骨2 Hz峰值4 000压力连续3 d(120转/d),测量2组尺骨相对矿化面积及相对骨形成率。结果负荷引起的骨形成在KO组小鼠中被抑制。与WT组相比,KO组小鼠的相对骨形成率降低约84%(P<0.01)。结论骨内Nrf2的失活将影响应力负荷所致的骨形成。Objective To investigate the role of nuclear factor（erythroid-derived 2）-like 2（Nrf2）in load-driven bone metabolism in Nrf2 knockout（KO）mice. Methods The hybridized mice in the same brood were selected through PCR detection and were divided into two groups,i.e.,the Nrf2 knockout（KO）group and the wild-type（WT）group. Ulna of mice was loaded with 4 000 peak microstrains at 2 Hz for 3 consecutive days（120 cycles/day）as scheduled,the relative mineralizing surface（r MS/BS）and the relative bone formation rate（r BFR/BS）of ulna were measured for the two groups. Results Load-induced bone formation was suppressed in KO mice. Compared to the WT control,the relative bone formation rate was roughly 84% lower in KO mice（P〈 0.01）. Conclusion The loss-of-function mutation of Nrf2 in bone diminishes load-driven bone formation.

关 键 词：核转录因子2 应力负荷 骨形成 

分 类 号：R493[医药卫生—康复医学]