Nrf2基因敲除抑制应力负荷下骨形成  

The inhibition effect of Nrf2 gene knockout on load-driven bone formation

作　　者：杨杨[1] 于爱文[1] 张佳星[1] 戴奇[1] 徐爱华[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,辽宁沈阳110001

出　　处：《解剖科学进展》2015年第3期282-284,287,共4页Progress of Anatomical Sciences

基　　金：沈阳市科技局基金项目(No.131882)

摘　　要：目的培养核转录因子2(Nrf2)基因敲除小鼠原代成骨细胞,研究Nrf2基因在应力所致骨形成中的作用。方法选取同窝杂交出生的幼鼠分为Nrf2基因敲出组(KO)及野生组(WT),在颅骨中分离出初级2成骨细胞,在平板流动腔中进行60 min的震荡流体剪切应力实验(12dynes/cm,Fluid Shear Stress FSS),后提取RNA,进行实时定量PCR分析Nrf2 m RNA。结果震荡60 min使野生组Nrf2m RNA的表达水平增加,但基因敲出组没增加。NAD(P)H醌氧化还原酶1(NQO1)m RNA和Wnt5a m RNA在Nrf2基因敲出组成骨细胞中的表达水平较野生组显著减少,而RANK配体m RNA表达水平显著上调。FSS也刺激WT组成骨细胞中Wnt3a和Wnt5a m RNA的表达,但是在Nrf2 KO组没有作用。结论 Nrf2基因敲出抑制成骨细胞的增长和活性。Objective To investigate the inhibition effect of Nrf2 gene knockout on load-driven bone formation metabolism in Nrf2 knockout（KO） mice primary osteoblast. Methods The hybridization Littermate 4.5-day-old mice were divided into Nrf2 knockout（KO） and wild type（WT） groups. The primary osteoblasts were isolated from calvarial bone, subjected to oscillatory fluid shear stress（FSS,12 dynes/cm2） in parallel plate flow chambers for 60 minutes at 37℃ using a previously described fluid flow device. The expression of Nrf2 mRNA in osteoblasts was determined by real-time PCR. Results The expression level of Nrf2 mRNA was upregulated following 60 minutes FSS in wild miee, but not increased in Nrf2 KO mice. The expression levels of NQO1 mRNA and WntSa mRNA in osteoblasts was significantly decreased in Nrf2 KO than in wild type, but Rank ligand mRNA level was significantly increased. FSS stimulated the expressions of Wnt3a and WntSa mRNA in wild-type osteoblasts, but not in Nrf2 KO osteoblasts. Conclusion The inhibition of Nrf2 gene knockout on osteohlast recruitment and activity indicates that Nrf2 gene promotes the growth of load-driven osteoblast.

关 键 词：核转录因子2 成骨细胞 基因敲出 小鼠 

分 类 号：R366[医药卫生—病理学]