Mitochondrial response in the rat focal cerebral ischemia

Abstract

Antecedents: focal cerebral ischemia (FCI) causes mitochondrial injure. Due to its participation in ATP production and in cell death processes, it is important to characterize the damage. Objetive: To show the tissue injures and mitochondrial proteomic profile changes in striatum and hippocampus in FCI. Material and methods: Fifteen min and 1h of FCI with and without 24h of sanguineous reperfusion (rpf) was induced in Male Wistar rats. Neurological evaluation, histological assessment and mitochondrial proteomic analysis was done. Results: Neurological deficit was observed from the 15 min of FCI. Tissue damage was observed with H&E stain; TTC stain show macroscopic cellular death at 1h-FCI/24h rpf. By proteomic strategy, 20 protein spots were initially found to be differentially expressed; 6 spots in striatum and 4 spots in hippocampus show qualitative differences, of these spots, two protein spots show evident changes from 15 min of FCI, in both cerebral regions. Conclusion: focal cerebral ischemia induces mitochondrial protein expression changes from the first minutes of the ischemic insult, as were observed by proteomic strategy. The subsequent identification and characterization of these proteins will allow studying the biochemical processes that take place in FCI, and will contribute to broaden the knowledge of the sequence of events that occur in response to ischemia.