心肌缺血再灌注损伤时细胞核内膜三磷酸肌醇受体变化的研究

Changes in inositol 1,4,5-triphosphate receptors in inner nuclear membrane of rat myocardium during ischemic reperfusion injury

目的 :研究心肌缺血再灌注损伤时细胞核内膜三磷酸肌醇 (IP3 )受体的改变。方法 :制作大鼠心肌缺血再灌注损伤模型。分离细胞核内膜 ,[3 H]IP3 配体受体结合实验分析心肌细胞核内膜IP3 受体与配体的最大结合容量(Bmax)和亲和力 (Kd)。测定不同浓度IP3 对4 5Ca2 + 转运的影响。结果 :心肌缺血再灌注损伤动物细胞核内膜IP3 受体与配体结合的Bmax是对照组的 1.78倍 (P <0 .0 1) ,但Kd无显著变化 (P >0 .0 5 ) ,IP3 受体对4 5Ca2 + 的转运也相应增加。结论 :在心肌缺血再灌注损伤时 ,IP3 受体上调 ,数目增多 ,对Ca2 + 的转运增加。

Objective:To investigate the changes in inositol 1,4,5-triphosphate receptors in inner nuclear membrane of rat myocardium during ischemic reperfusion injury.Methods:Rat model of ischemic reperfusion injury was prepared. The maximum binding site density(B max) and affinity(Kd) of IP 3 for inner nuclear membrane were measured by IP 3 binding assay during ischemic reperfusion injury. The function of IP 3 receptors to release Ca 2+ was measured by different concentrations of IP 3.Results:B max during ischemic reperfusion injury was 2.78 times higher than control(P<0.01),while no alteration of affinity of IP 3 receptors for ligands was found. Ca 2+ transferation to the inner membrane vesicle was also increased accordingly during ischemic reperfusion injury.Conclusions:Binding site density and the function of IP 3 receptors in inner nuclear membrane were progressively increased during myocardial ischemic reperfusion injury.