Tai K-K, Pham L, Truong D D
Long Beach Memorial Medical Center, Long Beach, CA 90806, USA.
Brain Inj. 2009 Dec;23(13-14):1081-8. doi: 10.3109/02699050903421123.
To investigate the role of ATP-sensitive potassium (K(ATP)) channels in the neuroprotective effects of a ketogenic diet against cardiac arrest-induced cerebral ischemic brain injury-induced neurodegeneration.
Male Sprague Dawley rats were randomly divided into three groups and were fed with a ketogenic diet for 25 days before being subjected to a cardiac arrest-induced cerebral ischemia for 8 minutes 30 seconds. Four hours before cardiac arrest-induced cerebral ischemia, one group was intracisternally injected with glibenclamide, a plasma membrane K(ATP) channel blocker. The second group was injected with 5-hydroxydecanoate, a mitochondrial K(ATP) channel blocker. The third group was without the pre-treatment with K(ATP) channel antagonist. Nine days after the cardiac arrest, rats were sacrificed. Fluoro-jade (FJ) staining was used to evaluate cerebral ischemic neurodegeneration in the rat brain sections.
The number of FJ-positive degenerating neurons in the CA1 area of the hippocampus, the cerebellum and the thalamic reticular nucleus of the ketogenic diet-fed rats with or without glibenclamide or 5-hydroxydecanoate pre-treatment before cardiac arrest-induced cerebral ischemia is zero.
The results suggest that K(ATP) channels do not play a significant role in the neuroprotective effects of the ketogenic diet against cardiac arrest-induced cerebral ischemic injury-induced neurodegeneration.
研究三磷酸腺苷敏感性钾（K(ATP)）通道在生酮饮食对心脏骤停诱导的脑缺血性脑损伤所致神经退行性变的神经保护作用中的作用。
雄性Sprague Dawley大鼠被随机分为三组，在经历8分30秒的心脏骤停诱导的脑缺血之前，给予生酮饮食25天。在心脏骤停诱导的脑缺血前4小时，一组经脑池内注射格列本脲（一种质膜K(ATP)通道阻滞剂）。第二组注射5-羟基癸酸（一种线粒体K(ATP)通道阻滞剂）。第三组未用K(ATP)通道拮抗剂进行预处理。心脏骤停9天后，处死大鼠。用荧光玉（FJ）染色评估大鼠脑切片中的脑缺血性神经退行性变。
在心脏骤停诱导的脑缺血前，无论是否用格列本脲或5-羟基癸酸预处理的生酮饮食喂养大鼠，海马CA1区、小脑和丘脑网状核中FJ阳性变性神经元的数量均为零。
结果表明，K(ATP)通道在生酮饮食对心脏骤停诱导的脑缺血性损伤所致神经退行性变的神经保护作用中不发挥重要作用。
