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Meloxicam attenuates brain cell injury following cerebral ischemia and reperfusion via down regulation of proinflammatory response

 
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Pathophysiology of Cell Injury Journal  Volume 2, Issue 1, pages 1-11 June 2013

Erik M. Loria; Cristina Schroeder; Polly Wallis; Michael B. Prendini

Abstract

Stroke is the major cause of death and disability worldwide, and the thrombolytic therapy currently available was unsatisfactory. Meloxicam is a non-steroidal anti-inflammatory drug (NSAID), and little is known regarding the effect of Meloxicam in acute cerebral ischemia. Here, we designed this study to investigate the potential protective effects of Meloxicam in cerebral ischemia induced by 60-minute of middle cerebral artery occlusion (MCAO) followed by reperfusion cell injury for 24-hr. C57Bl6/N mice were pretreated with Meloxicam or normal saline (control). Infarct volumes were determined using magnetic resonance imaging and tetrazolium staining. Immunofluorescence was performed to evaluate apoptosis of neuron cells. The expression levels of proinflammatory cytokines and PI3K/Akt pathway were detected by ELISA and Western blot respectively. The results showed that Meloxicam decreased cerebral ischemia, improved neurological function and attenuated cellular apoptosis in vascular endothelial cell. These findings suggest that Meloxicam may play a major role in neruoprotective following transient focal cerebral ischemia and   further studies will elucidate the effect of Meloxicam treatment on cell proliferation and behavioral outcome in moderate to severe ischemic injury in the brain.

Keywords: Meloxicam; Cerebral ischemia; Stroke; MCAO

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