周宇宏 周佳莹 王丽娟 李俊男.苦参碱对哇巴因诱导钠电流改变的调节作用[J].,2015,15(29):5609-5612 |
苦参碱对哇巴因诱导钠电流改变的调节作用 |
Modulation of Matrine on SodiumCurrent Induced by Ouabain |
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DOI: |
中文关键词: 苦参碱 哇巴因 钠离子通道 动作电位时程 |
英文关键词: Matrine Ouabain Na+ current Action potential duration |
基金项目:黑龙江省教育厅科研基金项目(12521175) |
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中文摘要: |
目的:探讨苦参碱拮抗哇巴因诱导的心律失常的作用机制。方法:应用全细胞膜片钳技术记录哇巴因对单个豚鼠心室肌细
胞的Na+电流和动作电位时程作用后,观察苦参碱对哇巴因诱导Na+电流和动作电位时程改变的恢复作用。结果:① 5 umol·L-1
哇巴因延长APD50 从给药前476 ± 40.7 ms 增加到744 ± 62.9 ms (n=6,P<0.05),APD90从给药前499 ± 84.9 ms 增加到775±
87.7 ms (n=6,P<0.01),100 umol·L-1苦参碱恢复APD50 至603 ± 79.0 ms (n=6, P<0.05),APD90 至630 ± 81.6 ms (n=6,P<0.05);
② 5 umol·L-1哇巴因可增加钠电流的峰值,在-20 mV 电压条件下,5 滋mol·L-1哇巴因增加INa,由正常-40.9 ± 2.32 pA/pF 增加到
-55.2 ± 2.26 pA/pF(n=8,P<0.05),100 umol·L-1苦参碱减少INa 至-34.6 ± 2.14 pA/pF(n=8,P<0.05);5 umol·L-1哇巴因右移钠通
道的激活曲线,并左移钠通道的失活曲线从而改变通道动力学特性;100 umol·L-1苦参碱可抑制哇巴因诱导的INa 的增加,并恢
复Na+通道动力学特性接近正常。结论:苦参碱拮抗哇巴因诱导的心律失常机制与其抑制哇巴因诱发细胞水平Na+电流的增加,
缩短哇巴因诱发APD 的延长有关。 |
英文摘要: |
Objective:To investigate the antiarrhythmic effects of matrine.Methods:Ouabain was used to construct an arrhythmic
model of cardiomyocytes, and the sodium current and action potential duration was recorded.Results:In cardiomyocytes of guinea pigs,
ouabain of 5 umol·L-1 prolonged APD50 from 476 ± 40.7 ms to 744 ± 62.9 ms (n=6, P<0.05) and APD90 from 499 ± 84.9 ms to
775 ± 87.7 ms(n=6, P<0.01), 100 umol·L-1matrine recovered APD50 to 603± 79.0 ms (n=6, P<0.05), APD90 to 630 ± 81.6 ms (n=6,
P<0.05) respectively. Ouabain of 1 umol·L-1 increased peak sodium currents by shifting the activation and inactivation curve. Ouabain of
5 umol·L-1 increased the peak of sodium current. At -20 mV, ouabain of 5 umol·L-1 increased INa, from -40.9 ± 2.32 pA/pF to -55.2 ±
2.26 pA/pF (n=8, P<0.05), 100 umol·L-1matrine decreased INa to -34.6 ± 2.14 pA/pF(n=8, P<0.05); matrine of 100 umol·L-1 recovered
the activation and inactivation curve to close to the normal level.Conclusion:Taken together, these findings provided the first evidence
that matrine could inhibit INa and shorten APD prolongation which contributed to its anti-arrhythmic effect. |
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