CAJ | 학술논문

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4000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。
목적：통과핵전록인자2（Nrf2）기인고제소서탐색Nrf2재응력소치골형성중적작용。방법통과PCR검측선취동와잡교출생적소서Nrf2기인고제（KO）조급야생（WT）조，안시급여척골2 Hz봉치4000압력련속3 d（120전/d），측량2조척골상대광화면적급상대골형성솔。결과부하인기적골형성재KO조소서중피억제。여WT조상비，KO조소서적상대골형성솔강저약84%（P<0.01）。결론골내Nrf2적실활장영향응력부하소치적골형성。
Objective To investigate the role of nuclear factor(erythroid?derived 2)?like 2(Nrf2)in load?driven bone metabolism in Nrf2 knock?out(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(rMS/BS)and the relative bone formation rate(rBFR/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.