替米沙坦对血管紧张素Ⅱ诱导的心肌细胞肥大及p-ERK_(1/2)的调节作用

Effects of Telmisartan on Activation of Extraceilular Signal-regulated Kinase_(1/2)(ERK_(1/2)) in Angiotensin Ⅱ Induced Cardiomyocyte Hypertrophy

观察替米沙坦（Telmisartan）对血管紧张素Ⅱ（AngⅡ）诱导的心肌细胞肥大及p-ERK1/2表达的影响.通过培养新生大鼠心肌细胞、用相差显微镜计数心肌细胞搏动频率、细胞图像分析系统测量细胞体积、考马斯亮蓝法测定心肌细胞总蛋白含量、[~3H]-亮氨酸掺入法测定蛋白合成速率作为心肌肥大指标;以ERK免疫沉淀活性试剂盒测定ERK活性;用Western-blot测定p-ERK1/2表达.实验结果显示Telmisartan能显著降低AngⅡ诱导的心肌细胞搏动频率、体积、总蛋白含量、蛋白合成速率上升,同时对p-ERK（1/2表达具有剂量、时间依赖性抑制作用.因此考虑Telmisartan可以抑制AngⅡ诱导的心肌细胞肥大,其机制与抑制p-ERK1/2表达有关.

Effects of Telmisartan on angiotensin II （Ang II ） induced cardiomyocyte hypertrophy and the expression of phosphorylated extracellular signal-regulated kinase1/2（p-ErK1/2） were observed. Total protein in the primary culture of neonatal rat cardiomyocytes was determined by Coomassie brilliant blue and protein synthesis rate was measured by [^3H]-Leucine incorporation. The expression of p-ERKI/z was assessed using Western blot and fluorescence microscope. Telmisartan can decrease Ang R-induced elevations of the total protein and protein synthesis rate;and inhibit the expression of p-ERK1/2 in a dose-and time-dependent manner. The results showed that Telmisartan significantly and dose dependently attenuated the ERK1/2 expression in the development of myocardial hypertrophy induced by Ang II . ERK1/2 may play an important role in cardiomyocytes hypertrophy induced by Ang II. The antihypertrophic effect of Telmisartan on cardiomyocyte hypertrophy induced by Ang II may be associated to it＇s effect of inhibit ion to ERK signaling pathway.