【摘要】 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。更多还原

【Abstract】 AIM : To investigate the effects of Ca 2+ /CaM dependent calcineurin(CaN) signaling pathway on cardiomyocytes hypertrophy of rat induced by neuropeptide Y(NPY). METHODS : Cardiomyocytes of neonatal Wistar rats were cultured with NPY of various concentrations (10,100 nmol·L -1 ). Cyclosporine A (CsA) was used to inhibit the activity of CaN. The methods of 3H Leu incorporation was used to assess protein synthesis rate in cardiomyocytes. Western blot and histochemistry were used to measure CaN protein expression and CaN activity in cardiomyocytes. RESULTS : 3 H Leu incorporation of cardiomyocytes were increased significantly by 100 nmol·L -1 NPY ( P < 0.05 ) and decreased by CsA. CaN activity and CaN α protein expression was elevated markedly in cardiomyocytes by 100 nmol·L -1 NPY ( P < 0.05 ). CONCLUSION : Neuropeptide Y activates Ca 2+ /CaM dependent calcineurin signal pathway,and CsA can inhibit cardiomyocytes hypertrophy induced by NPY. It indicates that Ca 2+ /CaM dependent calcineurin (CaN) signaling pathway plays an important role in cardiomyocytes hypertrophy of rats induced by NPY.更多还原