染氟大鼠血清中硬骨素表达水平及其在Wnt通路调控Runx2表达中作用的实验研究  

Study of the expression level of serum SOST and its role in regulating Runx2 expression on Wnt/β-catenin pathway in fluoride exposed rats

作　　者：李长城[1] 刘晓利[1] 刘克俭[1] 黄安斌[1] 崔彩岩[1] 刘芸[1] 余立凯[1] 张裕曾[1] 余达林[1] 

机构地区：[1]华中科技大学同济医学院,湖北武汉430030

出　　处：《工业卫生与职业病》2012年第3期157-161,共5页Industrial Health and Occupational Diseases

基　　金：国家自然科学基金资助项目(81072255)

摘　　要：目的观察染氟大鼠血清中硬骨素(SOST)、核心结合因子(Runx2)表达水平的变化,探讨SOST在经典Wnt通路调控Runx2表达中的作用。方法选取64只大鼠随机分为低剂量组(1.6mg/kgNaF)、中剂量组(16mg/kg NaF)、高剂量组(32mg/kg NaF)和对照组(0mg/kg NaF),每组16只,雌雄各半;采用微电极法进行尿氟、血氟测定;全自动生化分析仪测定血清中碱性磷酸酶(ALP)活力;ELISA试剂盒测定血清中SOST和Runx2。结果高剂量组在第35天时,SOST血清中浓度为(11.55±1.02)μg/L,表达开始下降;Runx2血清中浓度为(120.42±12.40)μg/L,表达开始升高;与对照组比较,差异有统计学意义(P<0.05)。第90天时,高、中剂量组SOST表达明显下降,Runx2表达明显升高,与对照组比较,差异均有统计学意义(P<0.01)。第90天时,大鼠体内SOST与Runx2表达水平呈负相关(r=-0.444,P<0.01)。结论高剂量的氟暴露可致大鼠体内SOST表达水平降低,Runx2表达水平升高;氟致骨损伤的发生可能与SOST的表达降低而对经典Wnt通路进行负调控,进而促进Runx2表达有关。Objective To observe the change of expression levels of serum SOST and Runx2 in fluoride exposed rats and to explore the role of SOST in regulating RunxZ on the classic Wnt/β-- catenin pathway. Methods 64 rats were randomly divided into four groups, 16 in each group and half and half in sex, i. e. low dose group（1.6 mg/kg NaF）, medium dose group（16 mg/kg NaF）, high dose group （32 mg/kg NaF） and the control group （0 mg/kg NaF）. The detection of urinary fluoride and blood fluoride were done by micro--electrode analysis. The ALP was tested by automatic biochemical analyzer and the expression of the serum SOST and Runx2 were determined by ELISA kit. Results On the 35th day, the level of serum SOST in high dose group was（ll. 55±1.02）μg/L, and the expression began to reduce; the serum Runx2 level was （120.42±12.40）μg/L, and the expression began to rise. Compared with the control group, the difference was significant（P〈0.05）. On the 90th day, serum SOST in high dose group and medium dose group obviously descended（P〈0.01）, and serum Runx2 significantly elevated（P〈0.01）. The expression of serum SOST was negatively associated with serum Runx2 （r=0. 444, P = 0. 000）. Conclusions Results suggest that the expression of serum SOST significantly descended and serum Runx2 obviously increased in high dose fluoride exposed rats. Fluoride induced bone injury may relate to the promotion of the Runx2 expression, which attributes to the negative regulation of the Wnt/？ -catenin pathway due to the reduction of SOST.

关 键 词：SOST 氟 Wnt信号通路 氟性骨损伤 

分 类 号：R135.1[医药卫生—劳动卫生]