Vitamin K3 inhibits mouse uterine contraction in vitro via interference with the calcium transfer and the potassium channels
Vitamin K3 inhibits mouse uterine contraction in vitro via interference with the calcium transfer and the potassium channels
复制标题
维生素 K3 通过干扰钙转移和钾通道在体外抑制小鼠子宫收缩
DOI：
10.1016/j.bbrc.2016.05.132
复制
发表时间：
2016-08-05
影响因子：
3.1
通讯作者：
Wang, Li
中科院分区：
文献类型：
--
作者：
Zhang, Xian-xia;Lu, Li-min;Wang, Li
以前的研究表明，维生素K3对平滑肌痉挛疾病有很大的缓解作用，但尚未有研究指出它在子宫中可能存在的抗收缩活性。在此，我们评估了维生素K3对子宫肌收缩力的影响，并探讨了维生素K3作用的可能机制。用肌图仪记录离体小鼠子宫条在组织浴中收缩力的变化。子宫条暴露于维生素K3或载体。维生素K3以浓度依赖的方式抑制自发收缩。它显著降低PGF2 α诱导的收缩频率，但不降低其幅度（58.0 μ M）。预先用维生素K3孵育降低了PGF2 α诱导的收缩的有效性。维生素K3的抗痉挛作用对钾通道阻滞剂（如四乙基铵、4-氨基吡啶、伊比利亚毒素）也敏感，但对一氧化氮相关通路阻滞剂不敏感。高浓度（29.0、58.0 μ M）的维生素K3可减弱Ca2+剂量反应，抑制1期收缩（细胞内储存钙释放）。这些数据表明，维生素K3通过影响钙和钾通道特异性地抑制子宫肌收缩性；因此，这种方法对子宫收缩活动相关疾病具有潜在的治疗作用。(C) 2016 Elsevier Inc.版权所有。
Previous studies have demonstrated vitamin K3 had a great relief to smooth muscle spastic disorders, but no researches have yet pinpointed its possible anti-contractile activity in the uterus. Here, we evaluated the effect of vitamin K3 on myometrial contractility and explored the possible mechanisms of vitamin K3 action. Myograph apparatus were used to record the changes in contractility of isolated mouse uterine strips in a tissue bath. Uterine strips were exposed to vitamin K3 or vehicle. Vitamin K3 suppressed spontaneous contractions in a concentration dependent manner. It significantly decreased the contractile frequency induced by PGF2 alpha but not their amplitude (expect 58.0 mu M). Prior incubation with vitamin K3 reduced the effectiveness of PGF2 alpha-induced contraction. The antispasmodic effect of vitamin K3 was also sensitive to potassium channel blockers, such as tetraethylammonium, 4-aminopyridine, iberiotoxin) but not to the nitric oxide related pathway blockers. High concentrations (29.0, 58.0 mu M) of vitamin K3 weakened the Ca2+ dose response and inhibited phase 1 contraction (intracellular stored calcium release). These dates suggest that vitamin K3 specifically suppresses myometrial contractility by affecting calcium and potassium channels; thus, this approach has potential therapy for uterine contractile activity related disorders. (C) 2016 Elsevier Inc. All rights reserved.