Abstract
Ischemic tolerance can protect the brain against cerebral ischemia and neurodegenerative diseases. However, several studies demonstrate ischemic tolerance by various methods, the exact mechanisms of ischemic tolerance has not been clearly understood.
In this study, we first studied brain ischemia-related mechanisms and then evaluated the outcomes of mitochondrial pathophysiology of ischemic tolerance in focal and full stroke animal models.
In this study, mitochondrial and peroxisomal reactions are considered critical in ischemic tolerance. In rats and Syrian mice, the middle cerebral artery occlusion (MCAO) model was employed to represent cerebrovascular stroke. Ischemic tolerance exhibits different types of adaptation responses associated with a number of sub-cellular changes.
Changes in the cellular non-genomic pathways are usually short and reversible; while, the consequences of genes expression are a long-term process and can lead to permanent alternations in the genes expression pattern. The ischemic tolerance can be clinically significant. Therefore, it is important to address the risks and advantages of ischemic tolerance in non-infarcted tissues such as transplanted ones
Keywords
Stroke Ischemia Neuroprotection Preconditioning Mitochondria
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© 2014, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.