Intracisternal administration of glibenclamide or 5-hydroxydecanoate does not reverse the neuroprotective effect of ketogenic diet against ischemic brain injury-induced neurodegeneration.

PRIMARY OBJECTIVE

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.

RESEARCH DESIGN

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.

MAIN OUTCOMES AND RESULTS

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.

CONCLUSIONS

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.