Protective effect of nitric oxide in aristolochic acid-induced toxic acute kidney injury: an old friend with new assets.

摘要: Aristolochic acid (AA) nephropathy (AAN), a progressive tubulointerstitial injury of toxic origin, is characterized by early and transient acute tubular necrosis. This process has been demonstrated to be associated with reduced nitric oxide (NO) production, which can disrupt the regulation renal function. In this study, we tested hypothesis that L-arginine (L-Arg) supplementation could restore function reduce after AA intoxication. C57BL/6 J male mice were randomly subjected daily i.p. injection either sterile saline solution or (2.5 mg kg(-1)) for 4 days. To determine whether AA-induced injuries linked NO L-Arg, substrate synthase, was supplemented (5%) in drinking water. Mice intoxicated exhibited features rapid-onset kidney injury, including polyuria, significantly increased plasma creatinine concentrations, proteinuria fractional excretion sodium (P < 0.05), along severe proximal cell NADPH oxidase 2 (Nox2)-derived oxidative stress 0.05). significant reduction bioavailability. L-Arg AA-treated bioavailability, turn improved (creatininaemia, proteinuria, excreted N-acetyl-β-D-glucosaminidase enzymuria) structure (tubular necrosis apoptosis). These changes reductions Nox2 expression production reactive oxygen species an increase antioxidant concentrations. Our results demonstrate preservation bioavailability leads protection reducing maintaining