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    Ozone treatment attenuates neuroinflammation and alters miRNA expression in a rat model of post-traumatic epilepsy
    (Springer Nature Link, 2026) Demir, Hüseyin; Demirtaş, Cumaali; Yıldırım, Hava; Demir, Ecem; Kıroğlu Uzun, Sezin; Şevgin, Kübra; Beyaztaş, Hakan; Güler, Eray Metin; Hekimoğlu, Gulam; Çoşkunpınar, Ender Mehmet; Şanlıer, Nafiye; Yıldırım, Mehmet
    The aim of this study was to investigate the effects of intraperitoneal ozone therapy in a post-traumatic epilepsy (PTE) model. An in vivo PTE model was established in male Sprague–Dawley rats, which were randomised to control (n=8), PTE (n=10), and PTE+Ozone (n=10) groups. 0.7 mg/kg ozone was administered intraperitoneally for 3 consecutive days. Seizure activity was video recorded for 120 min and evaluated for latency, frequency, duration, and severity. Behav ioral assessments of locomotor activity, anxiety, and spatial memory were conducted using open field, elevated plus, and radial arm maze tests on days 4–6 after the first ozone application. Blood and brain tissues were collected for biochemical assays (SUR1, TRPM4, IL-1β, IL-6, TNF-α, TAS, TOS, OSI, thiol–disulfide homeostasis), histological analyses (H&E, Cresyl Violet, and 8-OHdG immunostaining), and qRT-PCR of epilepsy-related miRNAs. Significant differences were observed among the groups for all serum and brain biomarkers (p<0.001). The PTE group showed marked increases in SUR1, TRPM4, IL-1β, IL-6, TNF-α, TOS, OSI, TT, NT, and DIS levels, accompanied by a decrease in TAS. Ozone treatment partially reversed these changes by reducing cytokine and oxidative stress markers, improving thiol–disulfide balance, and restoring TAS levels. Behavioural testing revealed beneficial effects of ozone, including reduced immobil ity, fewer errors in the radial arm maze, and increased open-arm exploration. Although seizure severity, latency, and duration were not significantly altered, seizure frequency showed a decreasing trend (p=0.067). Immunofluorescence for 8-OHdG revealed increased hippocampal oxidative DNA damage in the PTE group, which was attenuated following ozone treatment. Analysis of miRNA expression revealed downregulation in the PTE group, whereas ozone treatment resulted in overall upregulation. There was no statistically significant difference between miRNA expression results and the PTE+Ozone group (p=0.056–0.076). Ozone therapy mitigated oxidative stress and inflammation, improved redox homeostasis, enhanced cognitive and locomotor performance, and reduced hippocampal DNA damage in the PTE model. Furthermore, the observed upregulation of specific miRNAs following ozone treatment highlights a potential molecular mechanism contributing to its neuroprotective effects.
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    Therapeutic potential of alpha‑tocopherol in reducing oxidative stress and inflammatory damage after experimental traumatic brain injury and pentylenetetrazol‑induced seizures
    (Springer Nature Link, 2026) Demirtaş, Cumaali; Yıldırım, Hava; Demir, Hüseyin; Kıroğlu, Sezin; Şevgin, Kübra; Beyaztaş, Hakan; Güler, Eray Metin; Hekimoğlu, Gulam; Aykın, Uğur; Coşkunpınar, Ender Mehmet; Yıldırım, Mehmet
    The effects of alpha-tocopherol on seizure parameters, locomotor-cognitive functions, inflammatory response, oxidative stress response, histopathological changes, immunohistochemical parameters, and miRNA fold changes were investigated in rats with traumatic brain injury (TBI) and pentylenetetrazol (PTZ)-induced seizures. Sprague–Dawley male rats were randomly divided into three groups: Control (n = 8), TBI + PTZ (n = 10), and TBI + PTZ + tocopherol (n = 10). After inducing TBI in animals using the weight-drop method, increased post-injury seizure susceptibility was achieved by administering subconvulsive doses of PTZ. Saline was administered intraperitoneally to the control and TBI + PTZ groups for 6 days, while 500 mg/kg alpha-tocopherol was administered intraperitoneally to the TBI + PTZ + tocopherol group. Seizure intensity, sei zure frequency, and total seizure duration were significantly reduced in the TBI + PTZ + tocopherol group compared to the TBI + PTZ group (p < 0.05). No significant adverse effects related to TBI and PTZ were observed in the animals’ locomotor activity, anxiety-like behaviors, or learning and memory test outcomes. In the TBI + PTZ + tocopherol group, significant reductions were observed in inflammatory cytokine response, oxidative stress, and SUR1-TRPM4 channel activity compared to the TBI + PTZ group (p < 0.001). While degenerative and apoptotic neurons and the number of 8-OHdG-positive cells in the CA1 and dentate gyrus regions were limited in the TBI + PTZ + tocopherol group, downregulated miR-324-5p increased (p < 0.05). Alpha-tocopherol reduced the severity and duration of seizures, reduced oxidative stress and inflammation, and stabilized the thiol-disulfide balance. It also reduced degenerative cell structures and DNA damage in the cortex, hippocam pus, and dentate gyrus. In conclusion, the findings of this study suggest that alpha-tocopherol is a potential neuroprotective agent that modulates early epileptogenic network instability in TBI and seizure susceptibility through multiple pathways, including oxidative stress, inflammation, and ion channel regulation.