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Hum Exp Toxicol ; 38(6): 713-723, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30924375

RESUMO

Inflammation is one of the mechanisms involved in the acute kidney injury (AKI) caused by cisplatin (CP)-induced nephrotoxicity. Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl) has powerful antioxidant activity. We investigated its potential nephroprotective effects and the underlying mechanisms that may add further benefits to its clinical usefulness in a CP-induced AKI model. Male Swiss albino mice were divided randomly into four groups: control, CP (20 mg/kg intraperitoneally), tempol (100 mg/kg/day, per os) + CP, and tempol only treatments. Blood samples were collected to analyze renal function parameters. Immunoblotting and immunohistochemical analysis were used to assess the level and localization of inflammatory markers. Tempol afforded protection to animals from CP-induced elevation of inflammatory markers as indicated by reduced expression of nuclear factor-kappa B, cyclooxygenase-2, and tumor necrosis factor-α in kidney tissue. Histological findings and analysis of kidney function markers corroborated with these findings confirming a nephroprotective role for tempol. In conclusion, this study provides important evidence for the promising anti-inflammatory effects of tempol which appears to contribute significantly to its nephroprotective action.


Assuntos
Injúria Renal Aguda/tratamento farmacológico , Anti-Inflamatórios/uso terapêutico , Óxidos N-Cíclicos/uso terapêutico , Injúria Renal Aguda/induzido quimicamente , Injúria Renal Aguda/metabolismo , Injúria Renal Aguda/patologia , Animais , Anti-Inflamatórios/farmacologia , Antineoplásicos , Cisplatino , Óxidos N-Cíclicos/farmacologia , Ciclo-Oxigenase 2/metabolismo , Rim/efeitos dos fármacos , Rim/metabolismo , Rim/patologia , Masculino , Camundongos , NF-kappa B/metabolismo , Marcadores de Spin , Fator de Necrose Tumoral alfa/metabolismo
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