Artikel
The evaluation of neuroinflammatory mediators in human epileptic amygdala tissue
Evaluation der neuroinflammatorischen Mediatoren im humanen epileptischen Amygdala-Gewebe
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Autoren
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Maryam Khaleghi Ghadiri
- Universitätsklinikum Münster, Klinik für Neurochirurgie, Münster, Deutschland
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Ali Gorji
- Universitätsklinikum Münster, Klinik für Neurochirurgie, Münster, Deutschland
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Walter Stummer
- Universitätsklinikum Münster, Klinik für Neurochirurgie, Münster, Deutschland
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Sara Abdolahi
- Universitätsklinikum Münster, Klinik für Neurochirurgie, Münster, Deutschland
| Veröffentlicht: | 25. Mai 2022 |
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Gliederung
Text
Objective: Multiple lines of evidence support the key role of neuroinflammation in the pathogenesis of epilepsy and associated comorbidities. The main aim of this investigation was to study the role of different inflammatory pathways in human epileptogenesis
Methods: Using immunohistochemistry and PCR, we assessed cellular injury as well as apoptosis, and determined the expression of various inflammatory mediators in epileptic brain specimens resected during epilepsy surgery on 17 patients with medically intractable epilepsy (compared to autopsy control).
Results: Our preliminary findings have shown a significantly higher cell injury and apoptosis in the epileptic tissues compared to autoptic specimens. Moreover, immunohistochemical studies revealed significantly lower expressions of the excitatory amino acid transporter 1 (EAAT1), caspase 3, and glutamate GluR1 subreceptor in the epileptic amygdala compared to the control tissues. PCR analyses have shown significantly higher expressions of PPARγ, EAAT1, and EAAT2 as well as lower expressions of GluR2, NR1, mGluR1, GABARA1, GABAB3, and GAD65 in the epileptic tissues compared with the autoptic amygdala specimens. Furthermore, seizure duration plays a regulatory role in the expressions of euchromatic histone-lysine N-methyltransferase 2 (G9a), GFAP, and GABARA1.
Conclusion: Our data suggest that the modulation of neuroinflammation may be novel preventive and/or therapeutic strategies in the control of seizures.
