摘要
目的:探讨生长分化因子11(GDF11)对老龄鼠骨代谢的影响。方法:将20只18月龄C57BL/6J小鼠随机分为实验组(GDF11组)和对照组(Vehi组)(n=10),GDF11组按每天0.3 mg/kg的剂量腹腔注射GDF11,Vehi组注射等量生理盐水;连续注射4周后,分别检测其血、尿中骨代谢相关生化指标,并用Micro CT分析股骨的形态学指标。然后再取C57BL/6J小鼠的P1代骨髓间充质干细胞(BMSCs),并将其随机分为2组,分别用含GDF11为0(对照组)、30 g/mL(实验组)诱导培养3 d后,qRT-PCR检测Runx2、PPAR-γ、COL-1、OCN等成骨、成脂相关基因的表达水平。结果:GDF11干预可显著降低小鼠骨合成代谢的生化指标,并加重其股骨的骨质疏松(P<0.05)。体外实验结果显示,GDF11干预可显著降低小鼠BMSCs中Runx2、COL-1基因的表达水平(P<0.05),并显著上调其成脂相关基因PPAR-γ的表达水平(P<0.05)。结论:GDF11能够抑制老龄小鼠的骨形成。
AIM： To investigate the effect of GDF11 on bone metabolism of aged mice. METHODS：Twenty 18-month old C57 mice were randomly divided into GDF11 group（ 0. 3 mg·kg^（-1）·d^（-1） intraperitoneal injection,n = 10） and Vehi group（ equivalent physiological saline,n = 10）,4 weeks after intervention,biochemical marks of bone metabolism were tested and histomorphometric indexes of femurs were measured by microcomputed tomography.RESULTS： GDF11 decreased biochemical marks of bone formation including COL-1 and OCN; increased the expression of PPAR-γ; enhanced the histomorphologic indexes of osteoporosis of femurs. CONCLUSION： GDF11 inhibits bone formation of old mice.
出处
《牙体牙髓牙周病学杂志》
CAS
2017年第11期623-628,共6页
Chinese Journal of Conservative Dentistry
基金
国家自然科学基金(81570730)
