【摘要】 本研究观察了钙调神经磷酸酶（CaN）依赖的信号通路在血管紧张素Ⅱ（AngⅡ）诱导的大鼠心肌细胞肥大中的作用。在AngⅡ刺激的大鼠心肌细胞肥大模型上，应用环孢素A（CsA）阻断CaN通路，观察心肌细胞3H-亮氨酸掺入、CaN、MAPK及PKC活性的变化。结果表明，AngⅡ（10－7mol/L）刺激大鼠心肌细胞3H-亮氨酸掺入校对照组增高46％（P＜0．01），CsA（0．5－5μg/ml）可以浓度依赖性方式抑制AngⅡ刺激的心肌细胞3H-亮氨酸掺入；同时观察到AngⅡ刺激的大鼠心肌细胞CaN及PKC活性分别较对照组增高39％和280％（P＜0．001），CsA可明显抑制AngⅡ刺激的心肌细胞CaN活性增加，但对PKC活性没有明显影响。实验还观察到MAPK特异性抑制剂PD098059亦可显著抑制AngⅡ刺激的心肌细胞3H-亮氨酸掺入。结果提示，CaN依赖的信号通路可能在AngⅡ诱导的心肌细胞肥大中起重要作用。更多还原

【Abstract】 The Present study was undehaken to observe the role of calcineurin (CaN)dopndent siedng pathway in the angiotensin Ⅱ (Ang Ⅱ )-indued cedac myocytehpertrophy. In culthed myocedial cells of neonatal rats, Ang Ⅱ was used to stimulatehypertrophy and CaN-pathway blocked by CsA(an idsbitor of CaN). 3H-leucine incorporation, and achvihes of CaN, ndtogen-activated protein kinase (MAPK) and pforeinkinase C (PKC) were inveshgated. The results showed tha 3H-leucine incorporation ofAng Ⅱ -stimulated myOCrtal cens was 46% higher than control (P＜0.01), whichcould be inhibited by CsA (0.5 ~ 5 μg/ml) and PD098059(an ichbitor of MAPK). CaNand PKC ashvities of Ang Ⅱ -shmalated myocardial cells were 39% and 280% higherthan conbol (P＜0.001 ) respectively, while no siedcant increase in MAP achviheswas observed. CsA could reverse the incra of CaN activity, but had no det on PKC.It is concluded tha the CaN-dePendent signaling pathway rnay play an importan role inthe development of the Ang Ⅱ -induced edac rnyocpe hpertrophy.更多还原