Investigation of the effect of fucoxanthin on the hippocampus in rats with experimental diabetes induced by streptozotocin

The aim of the present study was to determine the effect of fucoxanthin (FX) on hippocampus damage caused by diabetes. In the study, 40 male Wistar albino rats weighing 220-250 g and aged 2-4 months were randomly divided into 5 equal groups (n=8) as Cont (Control), D (Diabetes), D+FX, FX and DMSO (dimethyl sulfoxide) (Solvent). A diabetes model was created by intraperitoneal administration of a single dose of 50 mg/kg streptozotocin (STZ) for groups D and D+FX. No other procedure was applied to rats in group D during the experiment, while 0.5 ml physiological serum was administered to rats in the Cont group, 50 mg/kg FX to rats in groups D+FX and FX, and 1 ml/kg 0.1% DMSO was administered intraperitoneally to rats in the DMSO group for 28 days. Learning tests were performed for the Barnes Maze test on days 16-20 of the 28-day study, and the results were obtained on day 28 and the animals were sacrificed on day 29. The brains of the rats, which were sacrificed after intracardiac blood was drawn under anesthesia, were removed, and the right hemisphere was blocked after routine histological follow-up. The sections were stained with cresyl violet for histopathological and stereological analyses and with Caspase-3 for immunohistochemical analyses. In addition, hippocampus volume was evaluated stereologically with Cavalieri principle. In addition, cytochrome (Cyt)-c, Annexin V, Caspase-3, Bax and Bcl 2 gene expressions were examined with molecular analyses for apoptosis in the left hemisphere. In addition, total antioxidant status (TAS) and total oxidant status (TOS) were measured in serum samples, and oxidative stress index (OSI) were calculated. As a result of the analyses obtained; In the D group, a decrease in the total hippocampus and CA1+CA2 region volume (p<0.01), irregularity in the arrangement of neurons and pyramidal cells with dark-stained cytoplasm were observed. In the D+FX group, these effects were reversed and an increase in hippocampus volume (p<0.01) and healthy neurons with regular borders were detected. In addition, molecular analyses revealed that the amount of diabetes-mediated apoptosis increased (p<0.05), and the Barnes Maze behavioral test revealed that diabetes caused memory impairment (p<0.01). In this context, it was determined that FX reduced oxidative stress in diabetes (p<0.01), improved impaired cognitive memory, decreased apoptosis and increased neuron survival. As a result; it was revealed that FX application significantly eliminated the deleterious effects of diabetes on the hippocampus.