白介素-2通过阿片κ受体抑制心肌细胞的收缩作用  

Interleukin-2 inhibited contractility of isolated ventricular myocytes via cardiac κ-opioid receptor pathway

作　　者：曹春梅[1] 夏强[1] 沈岳良[1] 陈莹莹[1] 徐万红[1] 

机构地区：[1]浙江大学医学院生理学教研室,浙江杭州310006

出　　处：《中国药理学与毒理学杂志》2001年第4期266-271,共6页Chinese Journal of Pharmacology and Toxicology

基　　金：浙江省自然科学基金青年人才专项资金资助(RC990 38)&&

摘　　要：本文采用酶解分离大鼠心室肌细胞 ,用视频跟踪系统测定单个心室肌细胞收缩 ,以研究白介素 2(IL 2 )对心肌细胞的作用及其机理 .结果发现 :①IL 2 (0 .5～ 2 0 0kU·L- 1)浓度依赖性地抑制成年鼠单个心室肌细胞的收缩 ;②纳洛酮 (10nmol·L- 1)和nor binaltorphimine(nor BNI,10nmol·L- 1)可阻断IL 2的收缩抑制作用 ;③百日咳毒素 (PTX ,5mg·L- 1)预处理后 ,取消了IL 2对心肌细胞收缩的抑制作用 ;④U7312 2预处理可阻断IL 2的收缩抑制作用 .结果表明 ,IL 2对酶解分离心室肌细胞收缩的抑制作用 ,是通过心肌细胞上κ阿片受体介导的 。The effect of interleukin 2(IL 2) on the contractility of enzymatically isolated ventricular myocytes and its possible mechanisms were investigated with the video tracking system. It was shown that IL 2 (0.5-200 kU·L -1 ) depressed the contractility of ventricular myocytes in a concentration dependent manner and pretreatment with the non selective opioid receptor antagonist, naloxone (10 nmol·L -1 ), or a specific κ opioid receptor antagonist, nor BNI (10 nmol·L -1 ), abolished the inhibitory effect of IL 2 on the contractility of cardiomyocytes. The effect of IL 2 was also canceled after pretreatment with pertussis toxin (PTX, 5 mg·L -1 ) as well as phospholipase C (PLC) inhibitor, U73122 (5 μmol·L -1 ). It is concluded that the depressant effect of IL 2 on the contractility of isolated ventricular myocytes is mainly mediated by cardiac κ opioid receptor pathway including a PTX sensitive Gi protein and PLC.

关 键 词：白细胞介素2 阿片受体 心肌细胞 收缩作用 G蛋白 磷脂酶C 

分 类 号：R965[医药卫生—药理学]