论文部分内容阅读
利用全细胞膜片钳技术,研究了稀土镧离子对非兴奋性小鼠成骨细胞(MC3T3)钙激活外向钾电流及其激活和失活动力学的影响.结果表明:MC3T3细胞钙激活外向钾电流随着电极内液中游离Ca2+浓度的增加而增加,且具有电压和胞内游离Ca2+依赖性特征.细胞外液中的稀土镧可浓度依赖性地抑制MC3T3细胞钙激活外向钾电流,其半数抑制浓度(EC50)为8.23±1.45μmol/L.50μmol/L氯化镧可使钾电流的激活曲线向正电位方向移动,而使其失活曲线向负电位方向移动,但对激活曲线和失活曲线的斜率因子k值影响都不大.研究表明:抑制钾通道电流,可使细胞膜去极化,细胞的兴奋性增加,从而增加胞外Ca2+向胞内流动,引起胞内Ca2+浓度的增加,由此而诱发一系列的生理和分子生物学事件.这一过程可能是稀土镧影响MC3T3成骨细胞生长和功能的分子作用机制之一.
The effect of rare earth lanthanum ions on calcium-activated outward potassium current and its activation and inactivation kinetics of non-excitatory mouse osteoblasts (MC3T3) was studied by whole-cell patch clamp technique.The results showed that calcium-activated potassium current The increase of free Ca2 + concentration in the electrode increased the voltage and the intracellular free Ca2 + -dependent characteristic.The rare earth lanthanum in the extracellular fluid inhibited the calcium-activated outward potassium current in MC3T3 cells in a concentration-dependent manner, and the half-inhibitory concentration (EC50) of 8.23 ± 1.45μmol / L.50μmol / L lanthanum chloride can make the potassium current activation curve to the positive potential direction, leaving the inactivation curve to the negative potential direction, but the activation curve and inactivation curve Of the slope factor k value is not large.Studies show that: inhibition of potassium channel current, membrane depolarization, increased cell excitability, thereby increasing the extracellular Ca2 into the intracellular flow, causing intracellular Ca2 + concentration increased from This led to a series of physiological and molecular biological events that may be one of the molecular mechanisms by which rare earth lanthanum affects the growth and function of MC3T3 osteoblasts.