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作 者:李丽婷[1] 朱亦堃[2] 郗光霞[2] 史书红[2] 毕晓燕[3] 李兴[2] 赵宝珍[2]
机构地区:[1]山西医科大学2008级硕士研究生山西医科大学第二医院,太原市030001 [2]山西医科大学第二医院内分泌科,太原市030001 [3]山西医科大学第二医院特需病房,太原市030001
出 处:《中华骨质疏松和骨矿盐疾病杂志》2010年第1期28-33,共6页Chinese Journal Of Osteoporosis And Bone Mineral Research
基 金:山西省卫生厅科技攻关计划项目(编号200911)
摘 要:目的研究不同浓度15d-PGJ_2对大鼠成骨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)及骨保护素(OPG)mRNA表达水平的变化,探讨PPARγ2内源性配体15d-PGJ_2对成骨细胞骨代谢相关基因表达的影响。方法体外培养大鼠成骨细胞,加入不同浓度15d-PGJ_2(0、10、20、30μmol/L)干预24小时后,采用逆转录PCR(RT-PCR)法检测成骨细胞PPARγ2、RANKL、ALP及OPG mRNA表达水平,比较不同浓度15d-PGJ_2对成骨细胞骨代谢相关基因mRNA表达的影响。结果不同浓度15d-PGJ_2呈剂量依赖性下调RANKL、ALP及OPG mRNA的表达水平,而呈剂量依赖性上调PPARγ2 mRNA的表达水平,组间比较差异有统计学意义(P<0.05,P<0.01)。结论 15d-PGJ_2可能通过激活PPARγ2转录活性抑制成骨基因mRNA的表达,参与增龄相关的骨质疏松的发病过程。Objective To observe the effect of 15-Deoxy- △12.14_prostaglandinj2 ( 15d_PGJ2 ) on the mRNA ex- pression of peroxisome proliferator activated reeeptorsγ2 ( PPARγ2), receptor activator of NF-KB ligand ( RANKL), al- kaline phosphatase (ALP) and osteoprotegerin (OPG) of osteoblastic cells, and study the effect of 15d-PGJ2 on bone metabolism. Methods Osteoblastic cells of Wistar rats were cultured in vitro and the fourth generation cells were select- ed to our study. The cells were cultured in DMEM with 15d-PGJ2 at different concentrations ( the final concentration is 0, 10, 20 and 30p, mol/L, respectively ) for 24h. RT-PCR was performed to semi-determine the mRNA expression of PPARγ2, RANKL, ALP and OPG. Results Semi-quantitative RT-PCR analysis showed that 15d-PGJ2 down-regulated the mRNA expression of RANKL, ALP and OPG, while it up-regulated the mRNA expression of PPARγ2 in a dose-de- pendent manner. Statistical significance was found in interclass comparison (P 〈 0. 05, P 〈 0. O1 ). Conclusion Our findings suggest that 15d-PGJ: suppress the expression of osteogenic genes through activating the transcription activity of PPARγ2, and it may be a plausible mechanism of senile osteoporosis.
关 键 词:过氧化物酶体增殖物激活受体Γ 15d—PGJ2 成骨细胞 骨质疏松
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