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目的:研究胡椒碱对H2O2引起的兔单个心房肌细胞内向整流钾电流(IK1)及超速激活的延迟整流钾电流(IKUr)异常的影响。方法:采用全细胞膜片钳技术分析50μmol/L H2O2对兔单个心房肌细胞IK1和IKUr的影响,并研究预先应用7μmol/L胡椒碱对其的保护作用。结果:7μmol/L胡椒碱对正常兔心房肌细胞IK1和IKUr及其通道动力学无显著影响。在50μmol/L H2O2作用下,兔心房肌细胞IK1峰值由(-148.2±16.7)pA/pF降低至(-64.2±9.8)pA/pF(P<0.05),电流-电压曲线上移;而IKUr峰值由(16.0±2.1)pA/pF降低至(6.1±1.4)pA/pF(P<0.05),电流-电压曲线下移,通道稳态激活曲线右移,通道稳态失活曲线左移及恢复时间减慢,而且存在频率依赖性特征。预先给予7μmol/L胡椒碱,明显减轻H2O2对IK1和IKUr的抑制作用(P<0.01),并可减少H2O2对超速激活延迟整流钾通道动力学的异常影响。结论:胡椒碱可减轻氧化应激对心房肌细胞IK1和IKUr的影响。
AIM: To investigate the effects of piperine on H2O2-induced inward rectifier potassium current (IK1) and ultra-delayed activated rectifier potassium current (IKUr) abnormalities in rabbit atrial myocytes. Methods: Whole cell patch clamp technique was used to analyze the effect of 50μmol / L H2O2 on IK1 and IKUr in single atrial myocytes of rabbits. The protective effect of 7μmol / L piperine was also studied. Results: 7μmol / L piperine had no significant effect on IK1 and IKUr in normal rabbit atrial myocytes and their channel dynamics. The peak value of IK1 in atrial myocytes was decreased from (-148.2 ± 16.7) pA / pF to (-64.2 ± 9.8) pA / pF (P <0.05) and the current-voltage curve shifted upwards in 50μmol / The peak value decreased from (16.0 ± 2.1) pA / pF to (6.1 ± 1.4) pA / pF (P <0.05), and the current-voltage curve shifted downwards and the steady-state activation curve shifted to the right. Recovery time is slow, and there are frequency dependent features. Pretreatment with 7μmol / L piperine significantly reduced the inhibitory effect of H2O2 on IK1 and IKUr (P <0.01), and decreased the abnormal effect of H2O2 on the kinetics of delayed rectifier potassium channel. Conclusion: Piperine can reduce the effects of oxidative stress on atrial myocytes IK1 and IKUr.