Protective effects of TREK-1 against oxidative injury induced by SNP and H2O2.

Aim: TREK-1 (TWIK-related K+ channel-1) is a 2-pore-domain K+ channel subtype. The present study investigated the role of TREK-1 in cell death induced by oxidative stress.

Methods: The cell viability of wild-type Chinese hamster ovary (CHO) and TREK-1-transfected CHO cells (TREK-1/CHO cells) was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in the presence of sodium nitroprusside (SNP) or hydrogen peroxide (H2O2).

Selective alteration of expression of Na+/Ca2+ exchanger isoforms after transient focal cerebral ischemia in rats.

The Na+/Ca2+ exchanger (NCX) is an antiporter located in the plasma membrane of many cells, which can maintain the intracellular Ca(2+) homeostasis. Some studies have shown the close relationship of NCX and cerebral ischemia. But controversial results were obtained.

[A simple and repeatable model of subarachnoid hemorrhage in rats].

Aim: To build a simple and repeatable animal model of subarachnoid hemorrhage (SAH).

Methods: SAH was produced by passing a nylon thread up through the right internal carotid artery and piercing a hole in the right anterior cerebral artery. At 12 h and 24 h after SAH operation, the rats were evaluated with rotarod test and the behavior scale (5-point scale).

Enhanced expressions of arachidonic acid-sensitive tandem-pore domain potassium channels in rat experimental acute cerebral ischemia.

To further explore the pathophysiological significance of arachidonic acid-sensitive potassium channels, RT-PCR and Western blot analysis were used to investigate the expression changes of TREK channels in cortex and hippocampus in rat experimental acute cerebral ischemia in this study. Results showed that TREK-1 and TRAAK mRNA in cortex, TREK-1 and TREK-2 mRNA in hippocampus showed significant increases 2 h after middle cerebral artery occlusion (MCAO). While the mRNA expression levels of the all three channel subtypes increased significantly 24 h after MCAO in cortex and hippocampus.