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

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.