Abstract：
BACKGROUND AND PURPOSE:The present study analyzed whether administration of sulindac, a non-steroidal anti-inflammatory drug (NSAID) would prevent, attenuate or repair ischemia induced brain injury and reverse functional impairment in a focal ischemia model of stroke. METHODS:Male Sprague-Dawley rats (weight 250-300 g) were subjected to middle cerebral artery occlusion (MCAO). Sulindac was given 2 days before and 24 h after ischemia at 0.2 mg/day with daily injections until sacrifice on day 3 or day 11. Infarct size was measured by TTC staining and western immunoblot was employed. RESULTS:TTC analysis of brain slices indicated a decrease in infarct size in sulindac treated animals. Western blot results indicated that sulindac induced expression of Hsp 27, a marker of cell stress, in the ischemic penumbra and core on days 3 and 11. Hsp 27 is important as a protective molecular chaperone. Increases were also found in the protective molecules Akt and Bcl-2 in the ischemic penumbra and core following sulindac administration. CONCLUSION:Our data indicate that administration of sulindac results in decreased infarct size and that there is a central role for the molecular chaperone Hsp 27, the pro-survival kinase Akt and the anti-apoptotic component Bcl-2 in mediating these protective effects.
journal_name
Brain Resjournal_title
Brain researchauthors
Modi JP,Gharibani PM,Ma Z,Tao R,Menzie J,Prentice H,Wu JYdoi
10.1016/j.brainres.2014.06.019subject
Has Abstractpub_date
2014-08-12 00:00:00pages
91-9eissn
0006-8993issn
1872-6240pii
S0006-8993(14)00835-Xjournal_volume
1576pub_type
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