Efeitos da Lectina de Dioclea Violacea na lesão renal aguda induzida por Isquemia/Reperfusão renal

Abstract

Acute kidney injury (AKI) is characterized by a rapid and potentially reversible decline in renal function; however, the current management for AKI is nonspecific and associated with limited supportive care. Considering the need for more novel therapeutic approaches, we believe that lectins from Dioclea violacea (Dvl), based on their anti-inflammatory properties, could be beneficial for the treatment of AKI induced by renal ischemia/reperfusion (I/R). Dvl (1 mg/kg, i.v.) or vehicle (100 µL) was administered to Wistar rats prior to the induction of bilateral renal ischemia (45 min). Following 24 hours of reperfusion, inulin and para-aminohippurate (PAH) clearances were performed to determine glomerular filtration rate (GFR), renal plasma flow (RPF), renal blood flow (RBF) and renal vascular resistance (RVR). Plasma urea, plasma creatinine and urine protein were analyzed by spectrophotometry. Renal inflammation was assessed using Myeloperoxidase (MPO) activity. Kidney sections were stained with hematoxylineosin to evaluate morphological changes. Intracellular superoxide anions, hydrogen peroxide, peroxynitrite, hildroxil radical, nitric oxide and apoptosis production in the kidneyswere analyzed using flow cytometry. I/R resulted in diminished GFR, RPF, RBF, and increased RVR plasma urea and plasma creatinine; however, these changes were ameliorated in rats receiving Dvl. There were no differences in urine protein levels between groups. AKI-induced histomorphological changes, such as tubular dilatation, tubular necrosis and proteinaceous casts, were attenuated by Dvl administration. Treatment with Dvl resulted in diminished renal MPO activity, oxidative stress and apoptosis in rats submitted to I/R. Our data reveal that Dvl has a protective effect in the kidney, improving renal function after IR injury, probably by reducing neutrophil recruitment and oxidative stress. These results indicate that Dvl can be considered a new therapeutic approach for AKI-induced kidney injury.