Thiamine alleviates cognitive impairment and epileptogenesis by relieving brain inflammation in PTZ-induced kindling rat model

ABSTRACT

Objective

Epileptogenesis, the process by which the brain becomes epileptic, is related to neuroinflammation, hyperexcitability cognitive deficits. Evidence suggests that improving brain inflammation can inhibit the epileptogenesis process and help the emergence of new drugs for the treatment of epilepsy. Therefore, the PTZ kindling model of epilepsy was utilized to assess the neuroprotective role of thiamine in epileptogenesis.

Methods

Male rats were exposed to PTZ-induced kindling and pretreated with low thiamine (25 mg/kg) or high thiamine (50 mg/kg). Cyclooxygenase (COX-1 and COX-2), interleukin 1-beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and nuclear factor-κB (NF-κB) concentrations in the brain were analyzed using biochemical assays. Cognitive function was evaluated using the passive avoidance test.

Results

Thiamine ameliorated epileptogenesis and enhanced the rats’ performance in the passive avoidance test. Also, thiamine significantly decreased the level of neuroinflammatory mediators in the brain induced by PTZ.

Conclusion

These results provide evidence that thiamine alleviates PTZ-induced neuroinflammation and cognitive impairments.

KEYWORDS:

• Epileptogenesis
• neuroinflammation
• thiamine
• rat

Acknowledgments

We would like to thank the Sivas Cumhuriyet University, School of Medicine, CUTFAM Research Center, Sivas, Turkey, for providing the necessary facilities to conduct this study.

Authors’ contributions

Sebahattin Karabulut contributed to the experimental design, statistical analysis, manuscript writing, and editing. Ahmet Kemal Filiz contributed to the experimental design and experimental procedures. Recep Akkaya contributed to the experimental design, biochemical analysis, and manuscript editing.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This research work was not funded by any public or private institution.