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目的:从电生理角度探讨葛根素抗心律失常的可能机制。方法:采用膜片钳技术记录大鼠心室肌细胞动作电位(AP)、转染的人胚胎肾细胞缓慢延迟整流钾电流(IKs),观察加药前、后葛根素对AP和IKs的影响。结果:0.01、0.1、1 mmol/L葛根素可浓度依赖性地延长动作电位时程,分别使APD50从(71.8±11.8)ms延长至(86.9±10.7)ms、(100.5±14.1)ms和(123.6±25.4)ms;使APD90从(164.6±21.4)ms延长至(188.3±11.5)ms、(221.6±25.7)ms和(278.7±38.2)ms(n=6,均P<0.05),而对RMP、APA和APD20无显著影响。此外,0.01、0.1、1 mmol/L葛根素对IKs抑制率分别为(17.8±2.5)%、(40.4±1.9)%和(60.9±3.2)%(n=6,均P<0.05)。结论:葛根素可能通过抑制IKs来延长动作电位时程,发挥抗心律失常作用。
Objective: To explore the possible mechanism of anti-arrhythmia of puerarin from electrophysiological point of view. Methods: The action potential (AP) of rat ventricular myocytes was recorded by patch-clamp technique. The delayed rectifier potassium currents (IKs) of transfected human embryonic kidney cells were observed. The effects of puerarin on AP and IKs were observed before and after dosing. Results: The concentrations of APD50 increased from (71.8 ± 11.8) ms to (86.9 ± 10.7) ms, (100.5 ± 14.1) ms and (100.5 ± 14.1) ms respectively in the concentration-dependent manner 123.6 ± 25.4) ms, and prolonged APD90 from (164.6 ± 21.4) ms to (188.3 ± 11.5) ms, (221.6 ± 25.7) ms and (278.7 ± 38.2) ms, respectively RMP, APA and APD20 had no significant effect. In addition, the inhibitory rates of puerarin at 0.01, 0.1 and 1 mmol / L on IKs were (17.8 ± 2.5)%, (40.4 ± 1.9)% and (60.9 ± 3.2)%, respectively (n = 6, all P <0.05). Conclusion: Puerarin may inhibit the IKs to extend the action potential duration, exert antiarrhythmic effect.