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目的:观察AMPK对血管内皮细胞中电导和小电导钙激活钾离子通道(K_(Ca)3.1和K_(Ca)2.3)表达和功能的影响。方法:应用人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)细胞系CRL-1730,通过Western blotting和real-time PCR等方法检测AMPK激活和下调对内皮细胞上K_(Ca)3.1和K_(Ca)2.3通道蛋白和m RNA表达的影响;分离大鼠肠系膜三级动脉,加入AMPK的激动剂或(和)抑制剂,应用微血管张力测定仪观察K_(Ca)3.1和K_(Ca)2.3通道介导的血管内皮舒张功能的变化。结果:激活AMPK可以上调血管内皮细胞K_(Ca)3.1和K_(Ca)2.3通道蛋白和m RNA的表达,其作用可被AMPK抑制剂逆转;应用RNA干扰技术下调AMPKα1亚基可以抑制K_(Ca)3.1和K_(Ca)2.3通道蛋白的表达。激活AMPK可以增强K_(Ca)3.1和K_(Ca)2.3介导的血管舒张功能,其作用可被AMPK抑制剂逆转。结论:AMPK对HUVECs上K_(Ca)3.1和K_(Ca)2.3通道的表达具有上调作用,该作用至少部分涉及转录水平的调节;AMPK对K_(Ca)3.1和K_(Ca)2.3通道介导的舒张功能具有上调作用。
AIM: To observe the effect of AMPK on the expression and function of conductance and small-conductance calcium-activated potassium channels (K_ (Ca) 3.1 and K_ (Ca) 2.3) in vascular endothelial cells. Methods: Human umbilical vein endothelial cells (HUVECs) cell line CRL-1730 was used to detect the effects of AMPK activation and down-regulation on the expressions of K_ (Ca) 3.1 and K_ (Ca) 2.3 and K (Ca) 2.3 channels in Ca2 + channels and Ca2 + channels and Ca2 + channels, Ca2 + channels and Ca2 + channels in Ca2 + Mediated Vascular Endothelial Dysfunction Changes. Results: Activation of AMPK upregulated the expression of K (Ca) 3.1 and K (Ca) 2.3 channel proteins and m RNA in vascular endothelial cells, and its effect could be reversed by AMPK inhibitor. AMPKα1 subunit could be inhibited by RNA interference ) 3.1 and K_ (Ca) 2.3 channel protein expression. Activation of AMPK enhances the vasodilatory function mediated by K_ (Ca) 3.1 and K_ (Ca) 2.3, and its effect can be reversed by AMPK inhibitors. CONCLUSION: AMPK up-regulates the expression of K (Ca) 3.1 and K (Ca) 2.3 channels on HUVECs, which at least partly involved in regulation of transcription. AMPK is mediated by K (Ca) 3.1 and K (Ca) The diastolic function has an upregulation effect.