血管钙化大鼠模型的肾脏损伤研究

目的观察血管钙化大鼠模型肾脏损伤及其病理变化。方法采用维生素D3（300000U／kg）和尼古丁（25mg／kg，溶于花生油）诱导大鼠血管钙化模型，以钙离子测试盒、碱性磷酸酶试剂盒测定钙含量和碱性磷酸酶（alkaline phosphatase，ALP）活性，以Von Kossa染色检测血管钙化程度；以肌氨酸氧化酶法检测大鼠血清肌酐浓度；苏木素伊红染色观察肾脏结构，Masson染色观察肾组织胶原的增生情况。结果血管钙化大鼠Von Kossa染色可见主动脉有大量黑色颗粒沉淀，表明有大量钙盐沉积；血管钙含量（0．410±0．0166）μmol·g^-1 vs.（0．270±0．019）μmol·g^-1，P〈0．05]、ALP活性（186．900±10．960）U·g^-1 vs.（119．100±8．646）U·g^-1，P〈0．05]、血清肌酐浓度（48．330±0．989）μmol／L憾（35．000±1．155）μmol／L，P〈0．05]较正常组升高，差异有统计学意义。苏木素伊红染色可见肾脏病理改变；Masson染色可见胶原增生。结论钙化大鼠肾功能和病理改变可能与肾脏纤维化、肾小球硬化及炎症因子等有关。

Injury of kidney in vascular calcification in rat model

Objectives To investigate the injury and pathology of kidney in aortic vascular calcification in rat model. Methods Aortic vascular model of SD rat was induced by Vitamin D3 （300 000 U/kg） plus nicotine （25 mg/kg, dissolved in peanut oil）. Vascular calcification was confirmed by Von Kossa staining. Calcium content and alkaline phosphatases （ALP） activity were detected by calcium assay kit and ALP assay kit respectively. Content of serum creatinine was determined by sarcosinc oxidase. Structure of kidney was observed by hematoxylin and eosin staining, and expression of collagen was determined by Masson staining. Results Von Kossa staining showed that there were black granules deposited in aortic wall of the vascular calcified rats. Calcium content （0.410±0.0166）μmol ·g^-1 vs. （0.270±0.019） μmol ·g^-1, p〈 0.05 ], ALP activity （ 186.900±10.960 ）U·g^-1 vs. （ 119.100±8.646 ）U·g^-1, P〈0.05 ] and serum concentration of creatinine （48.330±0.989） μmol/L vs. （35.000±1.155） μmol/L, P〈0.05] in calcified group were significantly higher than those in normal group. The pathology of renal changed in calcified group,while the expression of collagen was significantly upregulated. Conclusions The function and pathology of kidney change in aortic vascular calcification in rat model, which may be infected by renal fibrosis, glomerular sclerosis and inflammatory factor.