Blockade of the mitochondrial permeability transition pore diminishes infarct size in the rat after transient middle cerebral artery occlusion

Shohei Matsumoto, Hans Friberg, Michel Ferrand-Drake, Tadeusz Wieloch

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskriftPeer review

Sammanfattning

The mitochondrial permeability transition pore is an inducer of cell death. During the reperfusion phase after cerebral ischemia, calcium accumulates in mitochondria, and a burst of free radical formation occurs, conditions that favor the activation of the mitochondrial permeability transition pore. Here the authors demonstrate that a blocker of the mitochondrial permeability transition pore, the nonimmunosuppressive cyclosporin A analogue N-methyl-Val-4-cyclosporin A (10 mg/kg intraperitoneally), administered during reperfusion and at 24 hours of reperfusion, diminishes infarct size in a rat model of transient focal ischemia of 2 hours' duration. The mitochondrial permeability transition pore may be an important target for drugs against stroke.

Originalspråkengelska
Sidor (från-till)736-741
Antal sidor6
TidskriftJournal of Cerebral Blood Flow and Metabolism
Volym19
Nummer7
DOI
StatusPublished - 1999 juli 1
Externt publiceradJa

Ämnesklassifikation (UKÄ)

  • Neurovetenskaper

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