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作 者:周代星[1] 杨光田[1] 何雪心[2] 刘蔷[3]
机构地区:[1]华中科技大学附属同济医院急诊科,湖北武汉430030 [2]华中科技大学同济医学院药学院,湖北武汉430030 [3]湖北省新华医院中医科,湖北武汉430015
出 处:《中国中药杂志》2007年第18期1921-1924,共4页China Journal of Chinese Materia Medica
摘 要:目的:观察粉防已碱(tetrandrine,Tet)对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的心肌肥大及P-ERK1/2表达及活性的影响。方法: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]-亮氨酸掺人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,Western-blot测定p-ERK1/2表达。结果;Tet能显著抑制AngⅡ诱导的心肌细胞搏动频率、体积、总蛋白含量、蛋白合成速率的上升;对p-ERK1/2表达及活性具有剂量依赖性的抑制作用。结论:Tet可以明显抑制AngⅡ诱导的心肌肥大,机制与降低p-ERK1/2表达及活性有关。Objective: To observe effects of tetrandrine (Tet) on angiotensin Ⅱ (Ang Ⅱ)-induced cardiomyocyte hypertrophy and the activity and expression of phosphorylated ERK1/2 ( p-ERK1/2 ). Method: In the primary culture of neonatal rat cardiomyocytes, as indexes of cardiomyocyte hypertrophy, pulsation rate was measured under phase contrast microscope. Cell size was determined by cell morphology analytical system. The total protein was determined by coomassie brilliant blue and protein synthesis rate was measured by [^3H]-Leucine incorporation. ERK activity was measured by immuno-precipitation. The expression of p-ERK1/2 was assessed using Western blot. Result: Tet can decrease Ang Ⅱ-induced elevations of the pulsation rate, cell size, total protein and protein synthesis rate; inhibit the activity and expression of p-ERK1/2. Conclusion: The anti-hypertrophic effect of Tet on Ang Ⅱ-induced cardiomyocyte hypertrophy was associated with inhibition of ERKv2 signaling pathway.
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