转鲑鱼降钙素基因酵母及RANKL对大鼠血管平滑肌细胞体外钙化的影响

The Effect of Salmon Calcitonin Gene Transformed Yeast and RANKL on Calcification of Rat Aortic Vascular Smooth Muscle Cells in vitro

观察核因子kB受体激活物配体(RANKL)对大鼠血管平滑肌细胞体外钙化的调节作用,以及转鲑鱼降钙素基因酵母对RANKL调节作用的影响。体外培养大鼠血管平滑肌细胞,建立体外血管平滑肌细胞钙化模型,在培养介质中分别加入RANKL及转鲑鱼降钙素基因酵母蛋白上清液,观察细胞钙沉积、细胞碱性磷酸酶活性及骨钙素的变化情况。结果表明,RANKL促进钙化培养的大鼠血管平滑肌细胞的钙沉积、细胞碱性磷酸酶活性及骨钙素的表达,而转鲑鱼降钙素基因酵母能够抑制RANKL的促钙化作用。RANKL可能通过增加细胞碱性磷酸酶活性及骨钙素的表达从而促进血管平滑肌细胞向成骨细胞转化;转鲑鱼降钙素基因酵母可能通过OPG/RANKL/RANK途径抑制血管平滑肌细胞钙化。

To investigate the regulative effect of Receptor Activator of Nuclear Factor-kappa B Ligand（RAN- KL） on calcification of rat aortic v＇ascular smooth muscle cells（VSMC） in vitro, and the influence of salmon calcitonin transformed yeast （yAGA2-sCT） on RANKL. Results showed that Culture of rat aortic vascular smooth muscle cells（VSMCs） in vitro and establishment of a calcification model, RANKL and yAGA2-sCT were added into the culture media, the calcium deposition, alkaline phosphatase（AKP） activity, and alterations of expression of osteocalcin were examined. Results showed that RANKL promoted the calcium deposition, AKP activity, and the expression of osteocalcin in VSMC, whereas yAGA2-sCT inhibited the effects of RANKL. RANKL increased calcium deposition in VSMCs, possibly through increasing AKP activity and expression of osteocalcium and thus favored the transformation of VSMC to osteoblast, and yAGA2-sCT may inhibit VSMC calcification through the OPG/RANKL/RANK system.