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Journal of Southern Medical University ; (12): 208-218, 2007.
Artigo em Chinês | WPRIM | ID: wpr-298203

RESUMO

<p><b>OBJECTIVE</b>To investigate the changes in phosphorylated JAK2 and STAT3 protein expression of and cell apoptosis following focal cerebral ischemia-reperfusion injury in rats.</p><p><b>METHODS</b>A rat models of focal cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion using modified filament method. Immunohistochemistry and Western blot analysis were used to detect the expression of P-JAK2 and P-STAT3 proteins, and TUNEL assay was employed to examine the cell apoptosis.</p><p><b>RESULTS</b>P-JAK2 and P-STAT3 protein expression increased significantly after cerebral ischemia-reperfusion injury in rats. The immunoreactivity was prominent in the peripheral of the ischemic region and reached the peak level at 24 h of reperfusion, followed by slight decrement. The apoptotic cells increased obviously after cerebral ischemia-reperfusion injury, also reaching the peak level at 24 h of reperfusion.</p><p><b>CONCLUSION</b>The expression of phosphorylated JAK2 and STAT3 may be involved in the ischemic cellular events including apoptosis. JAK2/STAT3 signaling pathway plays a role in the pathophysiological process of cerebral ischemia/reperfusion cell injury and repair.</p>


Assuntos
Animais , Masculino , Ratos , Apoptose , Western Blotting , Imuno-Histoquímica , Marcação In Situ das Extremidades Cortadas , Infarto da Artéria Cerebral Média , Janus Quinase 2 , Metabolismo , Fosforilação , Ratos Sprague-Dawley , Traumatismo por Reperfusão , Genética , Fator de Transcrição STAT3 , Metabolismo
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