金属硫蛋白对心脏缺血再灌注损伤保护作用机制研究  

The study of cytoprotective effect mechanism of metallothionein on heart ischemia-reperfusin injury

作　　者：葛淑君[1] 仲崇霞[1] 程时[1] 

机构地区：[1]北京医科大学生物物理系,北京100083

出　　处：《中国药理学通报》2000年第3期265-268,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助课题 !No 39470 344

摘　　要：目的　观察并比较不同亚型金属硫蛋白 (MT)与心肌血管内皮细胞以及MT与缺血再灌注损伤后心肌血管内皮细胞的特异结合。方法　以胶体金为示踪物 ,采用离体心脏灌流模型 ,电镜下观察心肌血管内皮细胞对MT的特异结合。结果　不同亚型MT(MT 1,MT 2 )与心肌血管内皮细胞特异结合无明显差异。心脏缺血 30min和 6 0min后心肌血管内皮细胞仍能特异结合MT ,在心脏缺血 30min时 ,心肌血管内皮细胞特异结合MT的量与正常有氧灌注相比无明显差异 ,心脏缺血 6 0min时 ,心肌血管内皮细胞特异结合MT的量明显减少。结论　为进一步研究该蛋白生理功能及其应用提供重要依据。AIM To investigate specific binding of metallothionein(MT) isoforms on endothelial cellsand that of MT on ischemic myocardium endothelial cells. METHODS Using colloidal gold labelling and isolated heart perfusion technique, uptaking process of MT by endothelial cells of small vessels in myocardium was observed by electron microscopy. RESULTS There was no significantly difference in specifically bind endthelial cells between MT 1 and MT 2. After ischemia for 30 min and 60 min , MT can still specifically bind endthelial cells . Ischemia for 30 min, binding amount of MT on endthelial cells did not show significantly difference. However,ischemia for 60 min, produced a remarkable reduction of binding on endthelial cells. CONCLUSION It is very important for revealing MT biological function and clinical use.

关 键 词：心脏缺血 再灌注损伤 金属硫蛋白 保护作用 

分 类 号：R977.6[医药卫生—药品] R542.2[医药卫生—药学]