Ischemic postconditioning in the rat hippocampus: mapping of proteins involved in reversal of delayed neuronal death

In this study, transient forebrain ischemia was induced in male Wistar rats with subsequent 3 days of reperfusion (ischemia/reperfusion group) or 2 days of reperfusion followed by 5 min ischemia and another 1 day of reperfusion (postconditioning group) to assess an effect of delayed postconditioning...

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Published inArchives italiennes de biologie Vol. 148; no. 1; p. 23
Main Authors Nemethova, M, Danielisova, V, Gottlieb, M, Kravcukova, P, Burda, J
Format Journal Article
LanguageEnglish
Published Italy 01.03.2010
Subjects
Analysis of Variance
Animals
Antioxidants - metabolism
Apoptosis - physiology
bcl-2-Associated X Protein - metabolism
Brain Mapping
Cell Count - methods
Gene Expression Regulation - physiology
Hippocampus - physiopathology
Ischemia - pathology
Male
Neurons - pathology
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rats
Rats, Wistar
Reperfusion Injury - pathology
Superoxide Dismutase - metabolism
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Summary:In this study, transient forebrain ischemia was induced in male Wistar rats with subsequent 3 days of reperfusion (ischemia/reperfusion group) or 2 days of reperfusion followed by 5 min ischemia and another 1 day of reperfusion (postconditioning group) to assess an effect of delayed postconditioning applied two days after a previous lethal ischemic attack. We have examined immunoreactivity of antioxidant enzymes (MnSOD, CuZnSOD) and proteins related to apoptosis development (Bcl-2, Bax). Results of microdensitometric measurements from the vulnerable hippocampal CA1 region and relatively resistant dentate gyrus were compared to sham controls and identically, results of postconditioning group were compared to ischemic one. Our findings show protective effects of postconditioning in both brain regions examined, include increased expression of antioxidant enzymes, mainly CuZnSOD, what can be demonstrated by microdensitometric results: CuZnSOD density after ischemia and reperfusion was 6261.5 +/- 411.35; after postconditioning 9746.6 +/- 584.55. In addition, postconditioning prevents an excessive ischemia-induced increase of pro-apoptotic protein Bax (Bax density after ischemia and reperfusion was 3462.51 +/- 321.66; after postconditioning 1766.89 +/- 255.63).
ISSN:0003-9829