夹竹桃麻素对兔心房肌IK1氧化损伤的保护作用

Protective effect of apocynin on oxidative damage of inward rectifier potassium current in rabbit left atrial myocytes

目的探讨夹竹桃麻素(APO)对兔左心房肌细胞内向整流钾电流(IK1)的保护作用。方法运用低浓度(50μmol/L)的过氧化氢(H2O2)建立氧化应激模型。应用膜片钳全细胞技术,探讨APO(100μmol/L)对兔左心房肌细胞IK1及动作电位时程(APD)氧化应激损伤的保护作用。Western blot检测各组兔左心房中Kir2.1蛋白的表达。反转录聚合酶联反应(RT-PCR)检测兔左心房中的KCNJ2 mRNA表达。结果与对照组比较,低浓度H2O2(50μmol/L)组IK1峰值从(-182.2±15.6)pA/pF下降到(-119.3±8.9)pA/pF(P<0.05),APO(100μmol/L)组IK1峰值为(-175.3±15.2)pA/pF无差异;与H2O2组比较,H2O2(50μmol/L)+APO(100μmol/L)组IK1峰值恢复到(-160.5±13.5)pA/pF(P<0.05);APO使由于H2O2处理后减小的静息膜电位(RMP)绝对值及缩短的90%的APD(APD90)得以恢复;与对照组相比,H2O2组Kir2.1蛋白表达下降(P<0.05);与H2O2组相比,H2O2+APO组Kir2.1蛋白表达明显恢复(P<0.05);与对照组相比,H2O2组KCNJ2 mRNA表达下降(P<0.05);与H2O2组相比APO+H2O2组KCNJ2 mRNA表达恢复(P<0.05)结论APO对兔左心房肌细胞IK1具有保护作用。

AIM To study the protective effect of apocynin(APO)on oxidative stress damage of inward rectifier potassium current(IK1)in rabbit left atrial myocytes.METHODS We made the model of oxidative stress by low level H2O2(50μmol/L).The whole cell patch clamp technique was used to study the protective effect of APO on IK1 and action potential duration(APD)under oxidative stress injury.Real-time qPCR and Western blot were used to detect the expression of KCNJ2 at mRNA and Kir2.1 protein levels.RESULTS APO restored the peak current decreased by H2O2.APO also recovered the shortened resting membrane potential(RMP)and APD90 caused by H2O2.Compared with those in H2O2 group,the expression of KCNJ2 mRNA and the protein levels of Kir2.1 were increased(P<0.05),which could be recovered by APO+H2O2.CONCLUSION APO has some protective effect on IK1 in left rabbit atrial myocytes.