Browsing by Author "Kocamaz, E"

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    Cytotoxic Effects of Hypericum Perforatum on Glioblastoma Cells by Inducing Oxidative Stress, Autophagy and Apoptosis
    Mete, M; Unsal, UU; Collu, F; Aydemir, I; Kocamaz, E; Barutcuoglu, M; Gurcu, B; Karakayali, M; Tuglu, MI
    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 Nl/ml JWO. Group 3: T98 glioma cells treated with 6 Nl/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 Nl/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.
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    Histological and electroencephalographic demonstration of probiotic effect for reduce of oxidative stress and apoptosis in experimental traumatic brain injury
    Karakayali, EM; Kocamaz, E; Alpay, S; Onal, T; Oztatlici, M; Durusma, R; Ozel, HF; Mete, M; Barutcuoglu, M; Kutlu, N; Tuglu, MI
    BACKGROUND: The gut microbiota modulates nervous system function. In the literature, it has been shown that this modula-tion is used in many nervous system injuries through oxidative stress (OS) and apoptosis mechanisms. In this study, it was aimed to investigate the neuroprotective effects of probiotic (PB) treatment in a rat traumatic brain injury (TBI) model with histological and electroencephalographic (EEG) data.METHODS: Forty male Wistar albino rats were divided into four groups. Group 1 was the control group (CONTROL, n=10) and no trauma was applied. Group 2 was the trauma group with the weight-drop technique (TBH, n=10). Group 3 was the sham group (SHAM), (TBH+sterile saline [SS], n=10) rats were given 500 mu L of SS per day by oral gavage. Group 4 was the PB treatment group, (TBH+PB, n=10) rats were treated daily for 7 days with 500 mu L of PB oral gavage. Brain samples were collected 7 days after trauma. Histopathological evaluation of brain samples was done with HE. OS with Endothelial nitric oxide synthase, vascularization with Vascular Endothelial Growth Factor, gliosis with S100, and apoptosis with caspase 3 were evaluated immunohistochemically. Apoptotic index was determined with TUNEL. In addition, EEG and somatosensory evoked potential (SEP) recording findings were compared.RESULTS: It was determined by HE staining that there was a significant (P<0.001) damage in the TBI and sham groups compared to the control group. It was found that PB treatment provided a significant (P<0.01) improvement in the damage created. While OS (P<0.01), gliosis (P<0.01), and apoptosis (P<0.05) decreased with PB treatment, angiogenesis (P<0.01) increased. In support of these findings, in the software-mediated EEG and SUP examination; Delta wave power and theta/alpha ratio increased with TBI and de-creased with PB treatment.CONCLUSION: The results showed that PB treatment provided a significant improvement in rats by reducing OS, apoptosis, and gliosis and increasing vascularity. To the best of our knowledge in the literature, it was shown for the 1st time that histological results for the treatment of PB were supported by software-mediated EEG and SEP analysis.