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Penumbral neuropreservation mediated by decreased caspase‐9 activation with a‐EPO
Author(s) -
Price Chrystal Debra,
Chaparro Rafael Eduardo,
Chalavarya Swati,
Coppola Domenico,
Camporesi Enrico M.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1274-c
Subject(s) - penumbra , saline , medicine , apoptosis , erythropoietin , stroke (engine) , programmed cell death , caspase 3 , anesthesia , andrology , chemistry , ischemia , biochemistry , mechanical engineering , engineering
Apoptotic cell death in the region surrounding the initial necrotic injury after an ischemic stroke, referred to as the penumbra, develops over an extended period of time and is thought to peak days later. The aim of this study was to determine the effect of asialoerythropoietin (a‐EPO) on apoptotic‐specific cell death after ischemic brain injury in rats. Reversible middle cerebral artery occlusion (MCAO) was induced for 90 minutes, immediately followed by subcutaneous implantation of an osmotic mini‐pump (control=saline, experimental=a‐EPO, 20 μg/kg per day). On day 4, saline perfused brains were fixed in 10% formalin and immunohistochemically stained for active cleaved caspase‐9 (cc‐9). Levels of a‐EPO in CSF measured by an ELISA assay were significantly higher in the a‐EPO group (p<0.05, data not shown). A‐EPO resulted in an eight‐fold reduction in activated cleaved caspase‐9 cells in the penumbra, compared to saline controls (Table I. p<0.05, data represented as mean ± standard deviation). Quantitative analysis suggests that a‐EPO is capable of reducing the amount of apoptotic cell death in the surrounding penumbra region after an ischemic stroke injury to the brain. Research support provided by the Department of Anesthesiology, University of South Florida. Table I. p <0.05, mean ± standard deviation I p < 0.05, mean ± standard deviation