Browsing by Author "Collu F."

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    Effects of lacosamide “a novel antiepileptic drug” in the early stages of chicken embryo development
    (Springer Verlag, 2016) Mete M.; Gurcu B.; Collu F.; Unsal U.U.; Duransoy Y.K.; Tuglu M.I.; Selcuki M.
    Introduction: Antiepileptic drugs (AEDs) are teratogens and confer a risk of congenital malformation. The estimated prevalence of major congenital malformations such as cardiac defects, facial clefts, hypospadias, and neural tube defects in epileptic women is 4–10 %, which represents a two- to fourfold increase in pregnant women compared to the general population. However, there are no clear data for newer drugs. Lacosamide (LCM), a novel AED, is the first of the third-generation AEDs to be approved as adjunctive therapy for the treatment of partial-onset seizures. There are no data on the pharmacokinetics of LCM during pregnancy, and only some published data have reported on its effects during pregnancy. Methods: In this study, three different doses of LCM (0.12, 0.5, and 1.60 mg in 0.18 mL) were applied under the embryonic disks of specific pathogen-free Leghorn chicken embryos after a 30-h incubation. Incubation was continued for 80 h, at which time all embryos were evaluated macroscopically and microscopically. Results: There was growth retardation in all of the LCM-treated groups. Major malformations increased in a dose-dependent manner and were mostly observed in the supratherapeutic group. Conclusion: Based on our data, LCM may cause growth retardation or major congenital malformations. Nevertheless, more extensive investigations of its reliability are needed. © 2016, Springer-Verlag Berlin Heidelberg.
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    Neuroprotective effects of oleocanthal, a compound in virgin olive oil, in a rat model of traumatic brain injury
    (Turkish Neurosurgical Society, 2018) Mete M.; Aydemir I.; Unsal U.U.; Collu F.; Vatandas G.; Gurcu B.; Duransoy Y.K.; Taneli F.; Tuglu M.I.; Selcuki M.
    AIM: To evaluate the neuroprotective effects of deocanthal OC in a rat model of traumatic brain injury (TBI). MATERIAL and METHODS: Twenty-six adult male, Wistar albino rats were used. The rats were divided into 4 groups. Group 1 was the sham group (n = 5). Group 2 was the trauma group (n = 5) where rats were treated with 10 mg/kg saline intraperitoneally (IP) twice a day. Groups 3 and 4, rats were treated with 10 (group 3, n = 8) or 30 (group 4, n = 8) mg/kg OC IP twice a day. For each group, brain samples were collected 72 hours after injury. Brain samples and blood were evaluated with histopathological and biochemical methods. RESULTS: Histopathological evaluation revealed a significant difference between Group 2 and Group 4. Biochemical findings demonstrated that the oxidative stress index was highest in Group 2 and lowest in Group 4. CONCLUSION: OC has a protective effect on neural cells after TBI. This effect is achieved by reducing oxidative stress and apoptosis. © 2018 Turkish Neurosurgical Society.
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    Therapeutic effects of Lacosamide in a rat model of traumatic brain injury: A histological, biochemical and electroencephalography monitoring study
    (Elsevier Ltd, 2021) Mete M.; Alpay S.; Aydemir I.; Unsal U.U.; Collu F.; Özel H.F.; Duransoy Y.K.; Kutlu N.; Tuglu M.İ.
    Objective: Traumatic Brain Injury (TBI) is a major cause of death and disability worldwide, especially in children and young adults. TBI can be classified based on severity, mechanism or other features. Inflammation, apoptosis, oxidative stress, and ischemia are some of the important pathophys-iological mechanisms underlying neuronal loss after TBI. Lacosamide (LCM) is an anticonvulsant compound approved for the adjunctive treatment of partial-onset seizures and neuropathic pain. This study aimed to investigate possible neuroprotective effects of LCM in a rat model of TBI. Material and methods: Twenty-eight adult male, Wistar albino rats were used. The rats were divided into 4 groups. Group 1 was the control group (n=7). Group 2 was the trauma group (n=7) where rats were treated with 100 mg/kg saline intraperitoneally (IP) twice a day. Groups 3 and 4, rats were treated with 6 (group 3, n=7) or 20 (group 4, n=7) mg/kg Lacosamide IP twice a day. For each group, brain samples were collected 72 hours after injury. Brain samples and blood were evaluated with histopathological and biochemical methods. In addition, electroencephalograpy monitoring results were compared. Results: The immunoreactivity of both iNOS and eNOS (oxidative stress markers) were decreased with LCM treatment compared to trauma group. The results were statistically significant (***P<0.001). The treatments of low (56,17±9,69) and high-dose LCM (43,91±9,09) were decreased the distribution of HIF-1α compared to trauma group (P<0.01). The number of apoptotic cells were decreased with LCM treatment the difference between the trauma group and 20mg/kg LCM treated group (9,55±1,02) was statistically significant (***P<0.001). Malondialdehyde level was reduced with LCM treatment. MDA level was significantly higher in trauma group compared to LCM treated groups (***P<0.001). The level of Superoxide dismutase in the trauma group was 1,86 U/ml, whereas it was 36,85 U/ml in 20mg/kg LCM treated group (***P<0.001). Delta strength of EEG in 20mg/kg LCM treated group were similar to control group values after LCM treatment. Conclusion: No existing study has produced results suggesting that different doses of LCM has therapeutic effect against TBI, using EEG recording in addition to histological and biochemical evaluations in rats. © 2021 Elsevier Ltd
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    Genotoxic Effect, Oxidative Stress and Cell Death due to Metronidazole Application in Gills and Liver Tissues of Rainbow Trout (Oncorhynchus mykiss)
    (University of Tehran, 2022) Gurcu B.; Koca S.; Koca Y.B.; Collu F.; Ibrahim Tuglu M.
    In this study, the purpose was to investigate the histopathological, genotoxic effect, oxidative stress and cell death due to Metronidazole (MTZ), which is a 5-nitroimidazole compound, used widely for the treatment of anaerobic organism infections in fish and humans on gill and liver tissues of Oncorhynchus mykiss. Trout fishes were exposed to 5, 10, and 20 mg/L of MTZ in the aquariums for 2, 4 and 8 days. Staining technics namely H&E, NOS immunohistochemistry, and TUNEL were performed to determine histopathological changes, oxidative damage and apoptosis. Additionally, smear preparations were also prepared from gill blood for genotoxic evaluations. The organ damage started in the 2nd day with 5 mg/L MTZ application and effects increased per duration and dose-dependent manner. It was observed that the gills had the primary and secondary lamellae lengths, with formation of clavate lamellae, fusion in secondary lamellae, separation of epithelium and aneurysm. Regional necrosis, vacuolization of hepatocytes, pycnotic nucleus, enlarged sinusoids were also determined in the liver. NOS immunoreactivity increased with the inducible immunoreactivity (iNOS) that was more prominent when compared to the endothelial immunoreactivity (eNOS). Apoptotic immunoreactivity was higher in the 10 mg 8th day experimental group at liver and gills, and was lower 20 mg 8th day experimental group. When the gills and liver compared with each other, in all doses, immunoreactivity was lower in gills, compared with liver. Genotoxic examinations showed that both number of micro nucleated erythrocytes and nuclei abnormalities were higher in MTZ-treated groups. © 2022 University of Tehran. All rights reserved.
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    Cytotoxic Effects of Hypericum Perforatum on Glioblastoma Cells by Inducing Oxidative Stress, Autophagy and Apoptosis
    (Turkish Neurosurgical Society, 2025) Mete M.; Unsal U.U.; Collu F.; Aydemir I.; Kocamaz E.; Barutcuoglu M.; Gurcu B.; Karakayali M.; Tuglu M.I.
    AIM: To identify the autophagy mechanism T98 glioma cells. MATERIAL and METHODS: Three groups were created with T98 human glioblastoma cells; Group 1: T98 glioma cells without treatment (Control group). Group 2: T98 glioma cells treated with 3 µl/ml JWO. Group 3: T98 glioma cells treated with 6 µl/ml JWO. The cell proliferation, oxidative stress, types of cell death were studied at IC50 dose of JWO. RESULTS: The proliferation of glioma cells was inhibited in 5.296 µl/ml dose. JWO induced apoptosis in T98 glioma cells in comparison with the control and there was statistically significant difference (p<0.001). Apoptosis was analyzed via TUNEL method and results were checked by flow cytometry. We also investigated the effects of JWO on autophagy in T98 glioma cells by immunostaining LC3-II and MDC fluorescent stainings. The differences between JWO treated and control group were notably significant (p<0.001). The immunofluorescence staining resultsof LC3-II was confirmed by Western blotting analysis. CONCLUSION: JWO seems to be an effective treatment agent for glioblastoma. Not only does it induce apoptosis via oxidative stress but also affects the autophagy. The use of JWO in combination with other treatment options may increase the efficacy of treatment. © (2025), (Turkish Neurosurgical Society). All rights reserved.