RESUMO
The study investigated the effect of aminoguanidine (AG) on surgical brain injury (SBI) in rat. AG (75, 150 and 300 mg/kg, i.p.) was administered immediately following surgical resection. Using a SBI model, we found that AG (150 mg/kg) significantly reduced cerebral edema, while AG at the doses of 75 and 300 mg/kg had no effect. And AG (150 mg/kg) significantly reduced Evans Blue extravasation into brain tissue and improved the neurological outcome compared to control group. Moreover, the expression of TNF-alpha and nuclear factor-kappaB (NF-kappaB) mRNA and protein in brain tissue at the edge of the resection site increased at 24h after SBI, which could be significantly attenuated by the treatment with AG via RT-PCR and Western blots methods. Our results demonstrated that SBI causes increased brain edema, BBB disruption and inflammation along the periphery of the site of surgical resection, which could be significantly improved by the treatment of AG.
Assuntos
Edema Encefálico/tratamento farmacológico , Lesões Encefálicas/tratamento farmacológico , Encéfalo/cirurgia , Guanidinas/uso terapêutico , Fármacos Neuroprotetores/uso terapêutico , Animais , Barreira Hematoencefálica/efeitos dos fármacos , Barreira Hematoencefálica/fisiopatologia , Western Blotting , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Química Encefálica/efeitos dos fármacos , Edema Encefálico/etiologia , Edema Encefálico/metabolismo , Lesões Encefálicas/diagnóstico , Lesões Encefálicas/etiologia , Lesões Encefálicas/metabolismo , Encefalite/tratamento farmacológico , Azul Evans , Extravasamento de Materiais Terapêuticos e Diagnósticos , Guanidinas/administração & dosagem , Masculino , NF-kappa B/metabolismo , Fármacos Neuroprotetores/administração & dosagem , RNA Mensageiro/metabolismo , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fator de Necrose Tumoral alfa/metabolismoRESUMO
The study was performed to investigate the effects of bradykinin preconditioning on spinal cord ischemic injury using an in vivo transient spinal cord ischemia model in rats. Prior to ischemia, bradykinin was infused continuously via the left femoral artery starting 15min before ischemia. Neurological functions were evaluated for 7 days postoperatively using modified Tarlov's scores. Tarlov's score outcomes showed a marked improvement in the bradykinin group compared to the ischemia group. The blood-spinal cord barrier (BSCB) permeability was also decreased by bradykinin preconditioning after 72 h reperfusion focal spinal cord in rats, which was greatly reversed by B9430 (bradykinin B2 receptor antagonist). Immunohistochemical and Western blot analysis of spinal cords revealed a significant increase in basic fibroblast growth factor protein (bFGF) levels. The study demonstrated that bradykinin preconditioning induces protection against spinal cord ischemic injury, and this protection is likely due to the protection of the vasculature of the spinal cord and the promotion of neuronal survival.