不同浓度15d-PGJ2对骨髓细胞PPARγ2及骨代谢相关基因表达的影响  

Influence of different concentrations of 15-Deoxy-△^(12,14)-prostaglandin J_2 on PPARγ2 mRNA expression and bone metabolism related genes in bone marrow cells

作　　者：李丽婷[1] 朱亦堃[2] 郗光霞[2] 史书红[2] 李兴[2] 赵宝珍[2] 

机构地区：[1]山西医科大学2008级硕士研究生,太原030001 [2]山西医科大学第二医院内分泌科

出　　处：《中国骨质疏松杂志》2010年第9期632-635,共4页Chinese Journal of Osteoporosis

基　　金：山西省卫生厅科技攻关计划项目(200911)

摘　　要：目的观察不同浓度15d-PGJ2对大鼠骨髓细胞过氧化物酶体增殖物激活受体γ2(PPARγ2)及骨代谢相关基因核因子-κB活化受体配体(RANKL)、碱性磷酸酶(ALP)、骨保护素(OPG)、核因子-κB活化受体(RANK)及抗酒石酸酸性磷酸酶(TRAP)mRNA表达水平的变化,探讨PPARγ2内源性配体15d-PGJ2对骨髓细胞PPARγ2及骨代谢相关基因表达的影响。方法体外培养大鼠骨髓细胞,加入不同浓度15d-PGJ2(0、10、20、30μmol/L)干预24h后,采用半定量逆转录PCR(RT-PCR)检测骨髓细胞PPARγ2、RANKL、ALP、OPG、RANK、TRAPmRNA表达水平,比较不同浓度15d-PGJ2对骨髓细胞PPARγ2及骨代谢相关基因表达的影响。结果不同浓度15d-PGJ2呈剂量依赖性下调RANKL、ALP、OPGmRNA的表达水平,同时呈剂量依赖性上调PPARγ2、RANK、TRAPmRNA的表达水平,组间比较差异均有统计学意义(P<0.05,P<0.01)。结论 15d-PGJ2可能通过激活PPARγ2转录活性抑制骨髓细胞成骨细胞标记物基因的表达,促进破骨细胞标记物基因的表达,这可能是15d-PGJ2参与增龄相关的骨质疏松发生的原因之一。Objective To observe the effect of different concentrations of 15-Deoxy-△12,14 prostaglandinJ2 （15d-PGJ2 ） on peroxisome proliferator activated receptors-γ2 （PPARγ2） mRNA expression, and the mRNA expressions of bone metabolism related genes, including receptor activator of NF-kB ligand （RANKL） , alkaline phosphatase （ALP） , osteoprotegerin （OPG） , receptor activator of NF-kB （RANK） , and tartrateresistant acid phosphatase （TRAP） , in bone marrow cells. To study the effect of PPARγ2 ligand, 15d- PGJ2 , on the expression of PPARγ2 and bone metabolism related genes. Methods Rat bone marrow cells were cultured in vitro. Different concentrations of 15d-PGJ2 （0, 10, 20, 30 umol/L） were administered in cultures for 24 h. mRNA expressions of PPARγ2, RANKL, ALP, OPG, RANK, and TRAP were determined using semi-quantitative RT-PCR. The effect of different concentrations of 15d-PGJ2 on PPARγ2 and bone metabolism related genes was compared. Results The mRNA expressions of RANKL, ALP, and OPG were dose-dependently down-regulated by 15d-PGJ2. While the mRNA expressions of PPARγ2, RANK, and TRAP were up-regulated in a dose-dependent manner. Statistical significance was found among the groups （P 〈 0. 05, P 〈 0.01 ）. Conclusion 15d-PGJ2 inhibits the expression of osteogenie genes and promotes the expression of osteoclastogenesis genes through activating the transcription activity of PPARγ2. This may contribute a plausible mechanism of the genesis of senile osteoporosis.

关 键 词：过氧化物酶体增殖物激活受体Γ 15d—PGJ2 骨髓细胞 骨质疏松 

分 类 号：R681[医药卫生—骨科学] R977[医药卫生—外科学]