线粒体ATP敏感钾通道与钙激活钾通道激活对正常与缺血脑线粒体通透性转变的影响

EFFECT OF ACTIVATION OF MITOCHONDRIAL ATP SENSITIVE POTASSIUM CHANNEL AND CALCIUM ACTIVATED POTASSIUM CHANNEL ON THE PERMEABILITY TRANSITION OF MITOCHONDRIA FROM BOTH NORMAL AND ISCHEMIC RAT BRAIN

目的:明确线粒体ATP敏感钾通道与钙激活钾通道对正常和缺血脑线粒体渗透性转变的作用。方法:实验采用分光光度法,在分离的线粒体上分别观察两种线粒体钾通道激动剂对正常与缺血脑线粒体肿胀的影响。结果:在正常脑线粒体,diazoxide与NS1619能有效抑制由钙诱导的线粒体A520下降,但其效应可被atractyloside所阻断。与正常相比,缺血损伤后的脑线粒体在钙离子诱导下线粒体A520下降较快,diazoxide与NS1619仍可抑制由钙诱导的线粒体A520下降,其作用同样为atractyloside所阻断。结论:线粒体ATP敏感钾通道与钙激活钾通道激活在离体条件均具有保护脑线粒体的作用,其作用可能是通过影响线粒体通透性转变而实现。

Aim： To clarify whether the activation of mitochondrial ATP sensitive potassium channel and calcium activated potassium channd can influence the permeability transition of normal and ischemic brain mitochondria. Methods： spectrophotometry was used to deterrnine the effect of the two mitochondrial potassium channel agonists on the swelling of normal and ischemic brain mitochondria respectively. Results： In normal mitochondria, diazoxide and NS1619 could inhibit the decrease of calcium induced mitc;chondrial absorhanee at 520 nm（A520）, which were blocked by atractyloside. When compared with the normal mitochondria, mitochondrial A520 decrease in ischemic brain was even more rapid. Diazoxide and NS1619 could still inhibit the calcium induced mitochondrial A520 decrease, which were blocked by atractyloside. Conclusion： Activation of mitochondrial ATP sensitive potassium channel and calcium activated potassium channel can protect brain mitochondria in vitro probably via influencing the mitochondrial permeability transition.