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首页> 外文期刊>Cellular Physiology and Biochemistry >Synergistic Inhibition of Delayed Rectifier K+ and Voltage-Gated Na+ Currents by Artemisinin in Pituitary Tumor (GH3) Cells
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Synergistic Inhibition of Delayed Rectifier K+ and Voltage-Gated Na+ Currents by Artemisinin in Pituitary Tumor (GH3) Cells

机译：青蒿素在垂体肿瘤（GH3）细胞中协同抑制延迟整流器K +和电压门控Na +电流。

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>Background: Artemisinin (ART) is an anti-malarial agent reported to influence endocrine function. Methods: Effects of ART on ionic currents and action potentials (APs) in pituitary tumor (GH3) cells were evaluated by patch clamp techniques. Results: ART inhibited the amplitude of delayed-rectifier K+ current (IK(DR)) in response to membrane depolarization and accelerated the process of current inactivation. It exerted an inhibitory effect on IK(DR) with an IC50 value of 11.2 ?μM and enhanced IK(DR) inactivation with a KD value of 14.7 ?μM. The steady-state inactivation curve of IK(DR) was shifted to hyperpolarization by 10 mV. Pretreatment of chlorotoxin (1 ?μM) or iloprost (100 nM) did not alter the magnitude of ART-induced inhibition of IK(DR) in GH3 cells. ART also decreased the peak amplitude of voltage-gated Na+ current (INa) with a concentration-dependent slowing in inactivation rate. Application of KMUP-1, an inhibitor of late INa, was effective at reversing ART-induced prolongation in inactivation time constant of INa. Under current-clamp recordings, ART alone reduced the amplitude of APs and prolonged the duration of APs. Conclusion: Under ART exposure, the inhibitory actions on both IK(DR) and INa could be a potential mechanisms through which this drug influences membrane excitability of endocrine or neuroendocrine cells appearing in vivo.
机译：> 背景： 青蒿素（ART）是一种抗疟疾药物，据报道会影响内分泌功能。 方法： ART对垂体肿瘤（GH 3 ）细胞通过膜片钳技术进行评估。 结果： ART抑制了延迟整流器K + 电流的幅度（< i> I K（DR））响应膜去极化并加速了电流失活的过程。它对 I K（DR）具有抑制作用，IC 50 值为11.2μM，增强了 I K（DR）失活， K D 值为14.7μM。 I K（DR）的稳态失活曲线向超极化方向移动了10 mV。氯毒素（1 µM）或伊洛前列素（100 nM）的预处理不会改变ART诱导的GH 3对 I K（DR）的抑制作用单元格。 ART还降低了电压门控Na + 电流（ I Na ）的峰值幅度，其浓度依赖于失活速率的减慢。 KMUP-1是晚期 I Na 的抑制剂，可有效逆转ART诱导的 I Na 。在电流钳记录下，仅凭ART可以降低AP的幅度并延长AP的持续时间。 结论： 在ART暴露下，对 I 的抑制作用K（DR）和 I Na 可能是该药物影响体内出现的内分泌或神经内分泌细胞膜兴奋性的潜在机制。我>。

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