Abstract

Aim: Diabets mellitus is associated with impaired learning and memory. Neuroinflammation is a pathophysiological hallmark of diabetes which include production of cytokines. It was suggested that nitrative injury has been implicated in the pathophysiologic mechanism of diabetes. Nod-like receptor family pyrin domain-containing (NLRP) inflammasomes are important in the development of inflammatory response through production of IL-1β and IL-18. In the present study was aimed to examine the relationship between NLRP3, IL-1 β, nitrotyrosine levels and cognitive functions in diabetic rats. Material and Methods: The rats were randomly divided into 2 groups: control and diabetic. Diabetes was induced by a single intraperitoneal injection of 60 mg/kg of streptozotocin (STZ). Body weight and blood glucose level were measured until euthanasia. Morris water maze (MWM) was used to evaluate the cognitive function in rats. Hippocampal NLRP3, IL-1 β and nitrotyrosine levels were measured. Results: The results showed that the elevated blood glucose was obseved in diabetic group. NLRP3 and nitrotyrosine levels were found to be increased in hippocampus of diabetic rats. There was no statsitical significance in the hippocampal IL-1β level with diabetes. In the MWM, diabetic rats spent more time to find the submerged platform when compared with control rats, implying a significant impairment of learning and memory, and this impairment was found to be statistically signifcant at day 5. Conclusion: Our results indicate that STZ induced diabetes causes learning and memory impairment in rats probably by generating nitrosative stress and increasing NLRP3 level in the hippocampus.

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