质膜钠钙交换体抑制剂SEA0400对通透化H9c2心肌细胞线粒体效应的荧光分析
Fluorescence Analysis of the Mitochondrial Effect of a Plasmalemmal Na/Ca Exchanger Inhibitor, SEA0400, in Permeabilized H9c2 Cardiomyocytes.
作者信息
Namekata Iyuki, Hamaguchi Shogo, Iida-Tanaka Naoko, Kusakabe Taichi, Kato Keisuke, Kawanishi Toru, Tanaka Hikaru
机构信息
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University.
Department of Food Science, Otsuma Women's University.
出版信息
Biol Pharm Bull. 2017;40(9):1551-1555. doi: 10.1248/bpb.b17-00079.
We investigated the effect on mitochondrial Ca of SEA0400, an inhibitor of the Na/Ca exchanger (NCX) which reduces mitochondrial Ca overload during myocardial ischemia, in digitonin-permeabilized H9c2 cells expressing the mitochondrial-targeted Ca indicator, yellow cameleon 3.1. The elevation of mitochondrial Ca concentration caused by an increase in extramitochondrial Ca concentration was inhibited by carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP) or ruthenium red, but enhanced by CGP-37157, a mitochondrial NCX inhibitor. SEA0400 had no effect on mitochondrial Ca under normal and ischemic conditions. Thus, the mitochondria-protective effects of SEA0400 could be explained by inhibition of plasmalemmal NCX but not mitochondrial NCX.
我们在表达线粒体靶向钙指示剂黄变色龙3.1的洋地黄皂苷通透化H9c2细胞中，研究了钠/钙交换体（NCX）抑制剂SEA0400对线粒体钙的影响，该抑制剂可减轻心肌缺血期间的线粒体钙超载。线粒体外部钙浓度增加所引起的线粒体钙浓度升高，受到羰基氰化物对-（三氟甲氧基）苯腙（FCCP）或钌红的抑制，但受到线粒体NCX抑制剂CGP-37157的增强。SEA0400在正常和缺血条件下对线粒体钙均无影响。因此，SEA0400的线粒体保护作用可以通过抑制质膜NCX而非线粒体NCX来解释。
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