Naringin: an antioxidant that improves hepatic damage produced by experimental diabetes mellitus

PLAVNIK L; RODRÍGUEZ V. A; TOLOSA DE TALAMONI N

Bs As

Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017

Hepatic injury is a major complication of Type 1 Diabetes mellitus (DM1). Since naringin (NA) is a flavonoid with antioxidant properties, it might reduce hepatic complications in DM1. The aim of this study was to know the effect of NA on hepatic oxidative/nitrosative stress and apoptosis in a model of DM1. Two-month male Wistar rats were used: a) controls, b) diabetic rats (induced by 60 mg/kg b.w. streptozotocin: STZ), and c) STZ+NA: diabetic rats treated with NA (40 mg/kg b.w.). Animals were sacrificed at 30 days post-treatment, and serum glucose, HbA1c, insulin, triglycerides (TG), GOT and GPT were determined. Liver slices were stained with H&E for morphometric analyses. Total glutathione (GSH) content, superoxide anion (˙O2-) levels and superoxide dismutase (SOD) and catalase (CAT) activities from rat liver were measured by spectrophotometry. Nitrosative stress was evaluated by nitric oxide (NO) and nitrotyrosine content and inducible nitric oxide synthase (iNOS) protein expression. Apoptosis was evaluated by counting apoptotic nuclei and Fas, FasL and Bax protein expression. Results were evaluated by ANOVA and Bonferroni test. STZ rats presented higher levels of glycemia, HbA1c, TG, GOT and GPT, and lower insulin levels in relation to those from controls. Although NA treatment did not produce changes in glycemia, HbA1c and insulin, it decreased the levels of TG and transaminases. The cytoplasmic and nuclear areas of the hepatocytes in the STZ rats were higher. STZ rats showed increased apoptotic nuclei and protein expression of molecules involved in apoptosis. STZ rats exhibited GSH depletion and increased ˙O2- content and SOD and CAT activities. NA treatment normalized these parameters. NO content and iNOS protein expression were higher in STZ rats compared to controls, which were prevented by NA. In conclusion, NA would have the ability to prevent chronic liver injury triggered by DM1 due to its antioxidant, anti-nitrosative and antiapoptotic properties.