Özet:

Purpose: Diabetes mellitus is associated with learning and memory disorder. Neuroinflammation is a pathophysical sign of diabetes that involves the production of cytokines. Nitrative damage is said to be part of the pathophysical mechanism of diabetes. Nod-like receptor family pyrin domain-containing (NLRP) is important in the development of inflammatory response with the formation of inflammatory plasma IL-1β and IL-18. This study was aimed at studying the relationship between NLRP3, IL-1 β, nitrotirosin levels and cognitive functions in diabetic rats.  Tools and Methods: The rats were randomly divided into 2 groups: Control and Diabetes. Diabetes was created with single dose of streptozotosin (STZ) (60 mg/kg, intraperitoneal). The body weight and blood glucose levels were measured until the animals were sacrificed. The Morris Water Labyrinth (MWM) was used to evaluate cognitive functions. Hypokampal NLRP3, IL-1β and nitrotirosin levels were determined by the ELISA method.  The findings: Diabetic groups showed an increase in blood glucose levels. The levels of NLRP3 and nitrotirosin were found to increase in the hypokampus of diabetic rats. There were no statistically significant changes in the hypokampal IL-1β levels with diabetes. In the MWM test, diabetic animals spent more time finding the hidden platform compared to controls. This also showed that learning and memory were significantly deteriorated, and this disorder was statistically meaningful on the 5th day. Results: Our findings show that diabetes created with STZ is likely to cause learning and memory disorders in rats by increasing the level of NLRP3 in the hipocampus and by nitrosative stress formation.

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