Aspectos morfológicos e imunohistoquímico do cérebro de ratos diabéticos, induzidos pela estreptozotocina, após tratamento com melatonina

Abstract

It is known that the central nervous system is vulnerable to complications caused by diabetes. This complications leads to increased oxidative stress in the brain, resulting in damage to the cerebral cortex among other regions. Insulin and hypoglycemic agents are still the most widely used treatments, however, current research with an experimental model of diabetes suggests the use of antioxidants, such as melatonin. Thus, we tested the hypothesis that exogenous melatonin may decrease or prevent the effects of diabetes in the frontal cortex of rat brain. Fifty albino rats were divided into 5 groups: GC: rats without diabetes induction; GD: diabetic rats induced by streptozotocin; GDM: streptozotocin-induced and melatonin-treated diabetic rats; GDI: diabetic rats induced by streptozotocin and treated with insulin; GDMI: diabetic rats induced by streptozotocin and treated with melatonin and insulin simultaneously. Diabetes was induced by intraperitoneal administration of streptozotocin (60 mg/kg). Insulin (5 U/day) was administered subcutaneously and melatonin (10 mg/kg) by drinking water. Both treatments were performed for 30 days after induction. The animals' weight, the cytokines IL-6 and TNF-α, apoptosis, glycogen, and morphometry and histopathology of the frontal cortex were analyzed. The results showed that the cerebral cortex of the diabetic animals presented axonal degeneration, reduced number of neurons in the cortex, reduced glycogen, increased IL-6 and TNF-α expression, elevated apoptotic index, and reduced animal weight and the brain. Treatment with melatonin associated or not with insulin prevented such effects. Thus, we conclude that melatonin associated or not with insulin may be an alternative in preventing the effects of diabetes in the frontal cortex of the brain.