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作 者:付强[1] 王晓雨 莫陶然 FU Qiang;WANG Xiaoyu;MO Taoran(Heilongjiang University of Chinese Medicine,Harbin 150040,China)
出 处:《中医药学报》2021年第3期22-26,共5页Acta Chinese Medicine and Pharmacology
基 金:国家自然科学基金项目(81874426);黑龙江省博士后基金项目(LBH-Z18249);国家中医药管理局名老中医工作室项目。
摘 要:目的:基于膜片钳技术探讨尖叶假龙胆含药血清对心肌细胞I Ca-L离子通道的影响。方法:通过对各组I Ca-L电流密度的峰值的变化、不同去极化水平电流密度的改变,I-V曲线、激活曲线以及失活曲线的变化等证明心肌缺血再灌注损伤发生后心肌细胞离子通道发生变化,尖叶假龙胆含药血清干预后能够改变离子通道的变化。制备尖叶假龙胆含药血清。选取大鼠H9c2心肌细胞株,建立缺氧复氧心肌细胞损伤模型,实验分为空白组、模型组、尖叶假龙胆含药血清高、中、低剂量组,应用膜片钳技术观察尖叶假龙胆含药血清对心肌细胞I Ca-L离子通道的影响。结果:与模型组比较,尖叶假龙胆含药血清各剂量组能够升高损伤后不同去极化水平电流密度(P<0.05),下移I-V曲线,降低激活与失活半电压值,使激活曲线发生左移,失活曲线发生右移。结论:尖叶假龙胆可能通过影响L型钙离子通道稳定心肌细胞的电生理活动,对心肌缺血再灌注损伤心肌产生保护作用。Objective:To investigate the effect of serum containing Gentianella acuta on the I Ca-L ion channel of myocardial cells by patch clamp technique.The changes of peak value of I Ca-L current density,current density at different depolarization levels,I-V curve,activation curve and inactivation curve in each group were used to prove that the ion channel of myocardial cells changed after myocardial ischemia-reperfusion injury and the changes of ion channels could be changed after the intervention of serum containing medicine.Methods:The serum containing Gentianella acuta was prepared.The model of hypoxic reoxygenation myocardial cell injury was established by selecting rat H9c2 myocardial cell line.The experiment was divided into the blank group,the model group and the serum containing Gentianella acuta groups of high-dose,medium-dose and low-dose.The effect of serum containing Gentianella acuta on myocardial cells I Ca-L ion channel of myocardial cells were observed by patch clamp.Results:Compared to the model group,the serum containing Gentianella acuta groups could increase the current density of different depolarization levels(P<0.05),move down I-V curve,reduce the half voltage value of activation and deactivation,make the activation curve shift to the left and the deactivation curve shift to the right.Conclusion:Gentianella acuta may have a protective effect on myocardial ischemia-reperfusion injury by affecting the electro-physiological activity of L-type calcium channel.
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