The effect of hydroxytyrosol on NRF2 expression in rat pancreas, created diabetes mellitus with streptozotocin

Type 1 diabetes mellitus is a chronic disease in the islets of Langerhans, where it loses its ability to produce insulin as a result of the destruction of insulin-producing β cells. The aim of this study is to determine the expression changes of Nrrf2, one of the important proteins of antioxidant metabolism, in the rat pancreas where diabetes was induced by streptozotocin. Hydroxythyrosol is a natural-strong phenolic antioxidant found in olive and olive oil, the major degradation product of oleuropein. The animals used in the experiment were randomly divided into 4 groups as control, HT, STZ and STZ+HT. Diabetes was induced intraperitoneally by single dose (55 mg/kg) streptozotocin injection. Blood glucose values were measured 48 hours after STZ injection and those with ≥ 250 mg/dL were considered diabetic. HT (10 mg/kg/day) injection was administered intraperitoneally to HT and STZ+HT groups for 30 days. In addition to high blood sugar, STZ group animals showed a decrease in body weight, polyphagia and polydipsia. These effects were not found in the control and HT groups. In the STZ+HT group, less water consumption was observed in the animals compared to the STZ group with non-statistically significant weight loss. STZ+HT group rats were diabetic but their blood glucose levels decreased slightly although not significant. Histological examination of the islet histology of the control group, well-formed; diabetic rats showed markedly irregular island border and islet degeneration, while the round shape exhibited large size and normal structure. Diabetic rats showed islet cells with clear vacuoles in the cytoplasm consistent with hydropic degeneration, whereas decreased damage was observed in HT-treated diabetics. As a result of immunohistochemical studies, it was determined that Nrf2 expression was lower in HT treated diabetic animals compared to STZ group. This indicates that STZ has a protective effect of HT against damage to β cells. As a result, demonstrated that Nrf2 expression had a protective and antioxidant role of HT in the prevention of STZ-induced T1DM.