Celecoxib after the onset of reperfusion reduces apoptosis in the amygdala |
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Authors: | Sévan Kaloustian Boubacar P Wann Thierno M Bah Stéphanie Falcao Anne-Marie Dufort Philippe Ryvlin Roger Godbout Guy Rousseau |
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Institution: | Département de Pharmacologie, Université de Montréal, Montreal, QC, Canada. |
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Abstract: | Reperfused myocardial infarction induces an inflammatory response that is responsible for local and systemic alterations.
Among these, apoptosis observed in the amygdala following myocardial infarction has been pointed out as a consequence of such
an inflammatory process. We hypothesized that inhibition of the inducible inflammatory enzyme Cox-2 during the reperfusion
period may attenuate the apoptotic process in the amygdala. Anaesthetized rats were subjected to left anterior descending
coronary artery occlusion for 40 min, followed by reperfusion. The Cox-2 antagonist Celecoxib (3 mg/kg i.p.) was administered
10 min after the onset of the reperfusion period. After 72 h of reperfusion, infarct size was determined and the lateral and
medial amygdala were dissected from the brain. Infarct size was similar between untreated and Celecoxib-treated animals (40–45%
of the area at risk). Cox-2 expression was significantly reduced in both parts of the amygdala in the Celecoxib group. Apoptosis
regression was observed in the amygdala of the Celecoxib group as shown by decreased number of TUNEL positive cells and by
decreased of caspase-3 activation. Bax/Bcl-2 ratio was not significantly altered by Celecoxib while Akt activation was increased
in the lateral amygdala but not in the medial amygdala. This data indicates that inhibition of Cox-2 by Celecoxib is associated
with regression of apoptosis in the amygdala following myocardial infarction. |
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Keywords: | Celecoxib Myocardial infarction Reperfusion Amygdala Apoptosis |
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