Schisandrin B decreases the sensitivity of mitochondria to calcium ion-induced permeability transition and protects against ischemia-reperfusion injury in rat hearts
Schisandrin B decreases the sensitivity of mitochondria to calcium ion-induced permeability transition and protects against ischemia-reperfusion injury in rat hearts
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DOI：
10.1111/j.1745-7254.2007.00614.x
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发表时间：
2007-10-01
影响因子：
8.2
通讯作者：
Kam-Ming Ko
中科院分区：
文献类型：
--
作者：
Po-Yee Chiu;Hoi-Yan Leung;Kam-Ming Ko
目的：观察五味子乙素(Schisandrin B，Sch B)对正常和缺血再灌流(I-R)大鼠心肌线粒体对钙离子刺激的通透性转换(PT)敏感性的影响，以阐明五味子乙素(Sch B)保护心肌的分子机制。结果：心肌I-R损伤可增加线粒体对钙离子刺激的PT的敏感性。线粒体PT敏感性的增强与线粒体Ca~(2+)含量的增加以及体外活性氧化剂产生和体内细胞色素c释放的程度有关。Sch B对心肌I-R损伤的保护作用与降低心肌线粒体对Ca~(2+)刺激PT的敏感性是平行的，尤其是在I-R条件下。结论：Sch B可增强心肌线粒体对钙离子刺激的PT的抵抗力，对I-R所致的组织损伤具有保护作用。
Aim: In order to elucidate the molecular mechanism underlying the cardioprotection afforded by schisandrin B (Sch B), the effect of Sch B treatment on the sensitivity of mitochondria to Ca2+ -stimulated permeability transition (PT) was investigated in rat hearts under normal and ischemia-reperfusion (I-R) conditions. Results: Myocardial I-R injury caused an increase in the sensitivity of mitochondria to Ca2+ -stimulated PT in vitro. The enhanced sensitivity to mitochondrial PT was associated with increases in mitochondrial Ca2+ content as well as the extent of reactive oxidant species production in vitro and cytochrome c release in vivo. The cardioprotection afforded by Sch B pretreatment against I-R-induced injury was paralleled by the decrease in the sensitivity of myocardial mitochondria to Ca2+ -stimulated PT, particularly under I-R conditions. Conclusion: The results suggest that Sch B treatment increases the resistance of myocardial mitochondria to Ca2+ -stimulated PT and protects against I-R-induced tissue injury.