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ATP-dependent potassium channel blockade strengthens microglial neuroprotection after hypoxia-ischemia in rats.

Abstract：

:Stroke causes CNS injury associated with strong fast microglial activation as part of the inflammatory response. In rat models of stroke, sulphonylurea receptor blockade with glibenclamide reduced cerebral edema and infarct volume. We postulated that glibenclamide administered during the early stages of stroke might foster neuroprotective microglial activity through ATP-sensitive potassium (K(ATP)) channel blockade. We found in vitro that BV2 cell line showed upregulated expression of K(ATP) channel subunits in response to pro-inflammatory signals and that glibenclamide increases the reactive morphology of microglia, phagocytic capacity and TNFα release. Moreover, glibenclamide administered to rats 6, 12 and 24h after transient Middle Cerebral Artery occlusion improved neurological outcome and preserved neurons in the lesioned core three days after reperfusion. Immunohistochemistry with specific markers to neuron, astroglia, microglia and lymphocytes showed that resident amoeboid microglia are the main cell population in that necrotic zone. These reactive microglial cells express SUR1, SUR2B and Kir6.2 proteins that assemble in functional K(ATP) channels. These findings provide that evidence for the key role of K(ATP) channels in the control of microglial reactivity are consistent with a microglial effect of glibenclamide into the ischemic brain and suggest a neuroprotective role of microglia in the early stages of stroke.

journal_name

Exp Neurol

journal_title

Experimental neurology

authors

Ortega FJ,Gimeno-Bayon J,Espinosa-Parrilla JF,Carrasco JL,Batlle M,Pugliese M,Mahy N,Rodríguez MJ

doi

10.1016/j.expneurol.2012.02.010

subject

Has Abstract

pub_date

2012-05-01 00:00:00

pages

282-96

issue

1

eissn

0014-4886

issn

1090-2430

pii

S0014-4886(12)00069-6

journal_volume

235

pub_type

杂志文章

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