ObjectiveTo test how losartan inhibits the expression of a-SMA protein in Human Umbilical Vein Endothelial Cells (HUVECs), which stimulated by arecoline. And further to gain the possible pathogenesis of OSF.MethodsWith different concentrations (2.5,5,10,20,40,μg/ml) of arecoline stimulate HUVECs, respectively, after2days,4days,6days, detected the expression of a-SMA in HUVECs using the method of Western Blot. Then With certain concentrations (40μg/ml) of arecoline induce HUVECs,making different concentrations (10-6Mol/L,10-5Mol/L) of losartan stimulate HUVECs, respectively, after2days,4days,6days, detected the expression of a-SMA in HUVECs using the method of Western Blot.Results(1) After the HUVECs stimulated by various concentrations of arecoline in2days,4days,6days, there were a little expression of a-SMA detected by Western Blot in2day group, and there were more expression of a-SMA detected by Western Blot in4,6days groups.(2) With certain concentrations (40μg/ml) of arecoline induce HUVECs, making different concentrations of losartan stimulate HUVECs, for2days,4days,6days, respectively, the expression of a-SMA were inhibited in varying degrees.ConclusionsExposure of HUVECs to Arecoline can induce endothelial-to-mesenchymal transition, and make HUVECs express a-SMA. And AT1R inhibitor can inhibit this transition to some extent, which suggesting that AngⅡmay play an important role in the endothelial-to-mesenchymal transition induced by arecoline. |