枸橼酸双乙酯抗血管钙化及对Pit-1和CaSR的调控

血管钙化是影响尿毒症患者预后的重要因素。目前大量研究显示血管钙化与钙磷代谢紊乱、III型钠磷转运体（Pit-1）和钙敏感受体（CaSR）等诸多因素有关。近期国内外学者以及我们前期研究发现枸橼酸及其衍生物可抑制血管钙化的形成，但其确切机制尚不清楚。本项目通过体内和体外实验模拟尿毒症的生理环境，采用原子光谱联用技术、核素及荧光标记、放射性配体受体结合、RT-PCR、Western blot、ELISA等方法，从整体-细胞-分子层次，阐明枸橼酸双乙酯（Et2Cit）在尿毒症患者血管钙化中的作用。验证Et2Cit与磷结合，与磷竞争Pit-1上的结合位点以及炎性因子与CaSR的关系，探明Et2Cit抗血管钙化机制，为改善尿毒症患者预后提供新治疗方案。

Vascular calcification greatly contributes to the morbidity and mortality of patients with uremia. Calcium-phosphorus metabolism disorder, sodium-dependent phosphate cotransporter (Pit-1) and calcium-sensing receptor (CaSR) play roles in vascular calcification. At present scholors abroad and home notice that citric acid and its derivatives can inhibit the development of vascular calcification. But the mechanisms of such function are not completely known. For the function of diethyl citrate (Et2Cit) in vivo and in vitro, several methods were adopted including atomic spectroscopy, radionuclide and fluorescent labeling, radioligand receptor binding assay, RT-PCR, Western blot, ELISA ect. Our aims are to test Et2Cit which can bind with phosphorus and compete with Pit-1 and to identify the relationship between inflammation and CaSR. These findings may be used to further elucidate the mechanisms of vascular calcification and used as a potential treatment strategies for uremia patients.