目的 :探讨Ca2 + CaM依赖的钙调神经磷酸酶(CaN)途径在神经肽Y(NPY)诱导心肌细胞肥大中的作用。方法 :用NPY (10、10 0nmol·L-1)刺激WISTAR乳鼠心肌细胞 ,并用CaN特异性抑制剂环胞霉素A加以干预。应用3 H Leu掺入法测定心肌细胞蛋白质合成速率 ,用免疫印迹 (Western blot)和组织化学法分别测定心肌细胞内CaN α蛋白表达和CaN酶的活性。结果 :较高浓度NPY(10 0nmol·L-1)可明显增加心肌细胞3 H Leu掺入量(P <0 .0 5 ) ,加入CsA可阻断上述效应 ;NPY(10 0nmol·L-1)还可明显增加心肌细胞内CaN酶比活性 (P <0 .0 5 ) ,并刺激心肌细胞CaN α蛋白表达(P <0 .0 5 )。结论 :NPY可活化大鼠心肌细胞Ca2 + CaM CaN途径 ,而CaN特异性抑制剂环胞霉素A可抑制NPY诱导的心肌肥大 ,说明Ca2 + CaM依赖的钙调神经磷酸酶 (CaN)途径参与神经肽Y诱导的心肌细胞肥大效应。 AIM: To investigate the role of Ca2 + CaM-dependent calcineurin (CaN) pathway in neuropeptide Y (NPY) -induced cardiomyocyte hypertrophy. Methods: Wistar neonatal rat cardiomyocytes were stimulated with NPY (10, 10 nmol·L-1) and intervention with cyclosporine A, a CaN-specific inhibitor, was performed. The protein synthesis rate of cardiomyocytes was measured by 3 H Leu incorporation method. The expression of CaNα protein and the activity of CaN were determined by Western blot and histochemistry respectively. RESULTS: Higher concentrations of NPY (100 nmol·L-1) significantly increased 3 H Leu incorporation in cardiomyocytes (P <0.05), and the addition of CsA blocked the above effects. NPY (100 nmol·L-1) ) Also significantly increased the intracellular CaN specific enzyme activity (P <0.05) and stimulated CaNα protein expression in cardiomyocytes (P <0.05). CONCLUSION: NPY activates the Ca2 + CaM CaN pathway in rat cardiomyocytes, while CaN-specific inhibitor Cyclosporine A inhibits NPY-induced cardiac hypertrophy, indicating that Ca2 + CaM-dependent calcineurin (CaN) pathway is involved Neuropeptide Y - induced cardiomyocyte hypertrophy.