Blockade of the mitochondrial permeability transition pore diminishes infarct size in the rat after transient middle cerebral artery occlusion
(1999) In Journal of Cerebral Blood Flow and Metabolism 19(7). p.736-741- Abstract
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... (More)
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.
(Less)
- author
- Matsumoto, Shohei ; Friberg, Hans LU ; Ferrand-Drake, Michel LU and Wieloch, Tadeusz LU
- publishing date
- 1999-07-01
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Brain, Cyclosporin A, Mitochondria, Mitochondrial permeability transition, N-methyl-Val-4-cyclosporin A (MeValCsA), Neuronal death
- in
- Journal of Cerebral Blood Flow and Metabolism
- volume
- 19
- issue
- 7
- pages
- 6 pages
- publisher
- Nature Publishing Group
- external identifiers
-
- pmid:10413027
- scopus:0033495895
- ISSN
- 0271-678X
- DOI
- 10.1097/00004647-199907000-00002
- language
- English
- LU publication?
- no
- id
- b2d55303-5c3a-4597-bafe-90d97fc5f408
- date added to LUP
- 2019-06-13 16:40:44
- date last changed
- 2024-04-16 11:02:53
@article{b2d55303-5c3a-4597-bafe-90d97fc5f408,
abstract = {{<p>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.</p>}},
author = {{Matsumoto, Shohei and Friberg, Hans and Ferrand-Drake, Michel and Wieloch, Tadeusz}},
issn = {{0271-678X}},
keywords = {{Brain; Cyclosporin A; Mitochondria; Mitochondrial permeability transition; N-methyl-Val-4-cyclosporin A (MeValCsA); Neuronal death}},
language = {{eng}},
month = {{07}},
number = {{7}},
pages = {{736--741}},
publisher = {{Nature Publishing Group}},
series = {{Journal of Cerebral Blood Flow and Metabolism}},
title = {{Blockade of the mitochondrial permeability transition pore diminishes infarct size in the rat after transient middle cerebral artery occlusion}},
url = {{http://dx.doi.org/10.1097/00004647-199907000-00002}},
doi = {{10.1097/00004647-199907000-00002}},
volume = {{19}},
year = {{1999}},
}