Neuroprotective Effects of Anodal tDCS on Oxidative Stress and Neuroinflammation in Temporal Lobe Epilepsy
BIOMEDICINES, cilt.14, sa.1, 2025 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 14 Sayı: 1
- Basım Tarihi: 2025
- Doi Numarası: 10.3390/biomedicines14010023
- Dergi Adı: BIOMEDICINES
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Directory of Open Access Journals
- Ondokuz Mayıs Üniversitesi Adresli: Hayır
Özet
Background: Epilepsy affects over 50 million people worldwide, and about 30% remain drug-resistant-underscoring the urgent need for new therapies. This study evaluated the neuroprotective effects of anodal transcranial direct current stimulation (tDCS) in PTZ-induced epilepsy at acute and chronic stages in rats. Methods: Sixty male Wistar Albino rats (12 per group) were randomly assigned to five groups: control, acute epilepsy, acute epilepsy+ tDCS, chronic epilepsy, and chronic epilepsy+ tDCS. Behavioral tests-including the open-field, novel-object recognition, and Y-maze-assessed locomotion, recognition, and spatial memory. Hippocampal tissues were analyzed for oxidative stress markers (SOD, MDA), inflammatory cytokines (IL-1 beta, TNF-alpha), histopathology, and mechanistic markers of astrocytic and nitric oxide-mediated neuronal damage (GFAP and nNOS immunohistochemistry). Results: PTZ-induced epilepsy resulted in cognitive deficits, increased oxidative stress, neuroinflammation, neuronal degeneration, and astrocytic activation. Specifically, SOD decreased, while MDA, IL-1 beta, and TNF-alpha increased; GFAP and nNOS upregulation indicated activation of astrocytes and nitric oxide-mediated neuronal damage. tDCS mitigated these effects by enhancing SOD, reducing MDA, IL-1 beta, and TNF-alpha, and modulating the NO/GFAP axis, which corresponded to decreased neuronal degeneration and vascular hyperemia. Behaviorally, tDCS improved recognition memory and partially rescued spatial memory deficits. Conclusions: Anodal tDCS exerts neuroprotective effects in acute and chronic epilepsy by modulating oxidative stress, neuroinflammation, and the astrocytic/nitric oxide pathways, supporting its potential as a non-invasive adjunct therapy for cognitive and cellular protection. Future studies should investigate its effects on hippocampal glutamatergic and GABAergic pathways, as well as calcium homeostasis.