Inhibition of mitochondrial permeability transition pore opening contributes to the neuroprotective effects of ischemic postconditioning in rats
- 1 February 2012
- journal article
- Published by Elsevier BV in Brain Research
- Vol. 1436, 101-110
- https://doi.org/10.1016/j.brainres.2011.11.055
Abstract
No abstract availableKeywords
Funding Information
- National Natural Science Foundation of China (30930091, 30725039)
This publication has 30 references indexed in Scilit:
- Attenuation of renal ischemia–reperfusion injury by postconditioning involves adenosine receptor and protein kinase C activationTransplant International, 2010
- What is the mitochondrial permeability transition pore?Journal of Molecular and Cellular Cardiology, 2009
- Preconditioning and tolerance against cerebral ischaemia: from experimental strategies to clinical useThe Lancet Neurology, 2009
- Cellular and Molecular Neurobiology of Brain PreconditioningMolecular Neurobiology, 2009
- Phosphate Is Essential for Inhibition of the Mitochondrial Permeability Transition Pore by Cyclosporin A and by Cyclophilin D AblationPublished by Elsevier BV ,2008
- Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell deathNature, 2005
- S-15176 inhibits mitochondrial permeability transition via a mechanism independent of its antioxidant propertiesEuropean Journal of Pharmacology, 2003
- Incomplete Infarct and Delayed Neuronal Death After Transient Middle Cerebral Artery Occlusion in RatsStroke, 1997
- Evidence for the presence of a reversible Ca2+-dependent pore activated by oxidative stress in heart mitochondriaBiochemical Journal, 1987
- A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye bindingAnalytical Biochemistry, 1976