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Journal of Southern Medical University ; (12): 528-530, 2009.
Artigo em Chinês | WPRIM | ID: wpr-233743

RESUMO

<p><b>OBJECTIVE</b>To investigate the role of sodium cromoglycate in brain protection and its effects on brain tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) expressions after global cerebral ischemia-reperfusion (IR) injury in gerbils.</p><p><b>METHODS</b>Twenty-four healthy male gerbils were randomized into 3 equal groups, namely the sham-operated group with isolation of the bilateral carotid arteries but without occlusion, IR injury model group with bilateral carotid artery occlusion, and sodium cromoglycate treatment group with bilateral carotid artery occlusion and sodium cromoglycate administration at 25 mg/kg via the lingual vein as soon as the reperfusion start with another dose 1 h later. The animals were then sacrificed and the thalamus were removed, fixed in 10% formaldehyde and sliced for observation under light microscope with HE staining. The rest brain tissues were prepared into homogenate to determine the content of TNF-alpha and IL-1beta. The right hemispheres of the gerbils were measured for wet weight and dry weight to calculate the water content in the brain.</p><p><b>RESULTS</b>The water content in the brain of the gerbils in the model group was the highest among the groups, and that in sodium cromoglycate treatment group was significantly less than that of the model group (P<0.05). Microscopic examination showed the most severe brain tissue damage in the model group with also the highest TNF-alpha and IL-1beta levels in the brain. The brain TNF-alpha and IL-1beta levels in sodium cromoglycate group were significantly decreased as compared with those in the model group (P<0.05).</p><p><b>CONCLUSION</b>Sodium cromoglycate can alleviate brain IR injury possibly by lowering the TNF-alpha and IL-1beta levels in the brain tissues.</p>


Assuntos
Animais , Masculino , Isquemia Encefálica , Metabolismo , Cromolina Sódica , Farmacologia , Gerbillinae , Interleucina-1beta , Metabolismo , Fármacos Neuroprotetores , Farmacologia , Distribuição Aleatória , Traumatismo por Reperfusão , Fator de Necrose Tumoral alfa , Metabolismo
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