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    The effect of the HMGB1/RAGE/TLR4/NF-?B signalling pathway in patients with idiopathic epilepsy and its relationship with toxoplasmosis
    (Wiley, 2024) Soyturk, Hayriye; Onal, Cansu; Kilic, Umit; Turkoglu, Sule Aydin; Ayaz, Erol
    This study aims to investigate the relationship between toxoplasmosis and this pathway, which may be effective in the formation of epilepsy by acting through the HMGB1/RAGE/TLR4/NF-kappa B signalling pathway in patients with idiopathic epilepsy. In the study, four different experimental groups were formed by selecting Toxoplasma gondii IgG positive and negative patients with idiopathic epilepsy and healthy controls. Experimental groups were as follows: Group 1: Epilepsy+/Toxo- (E+, T-) (n = 10), Group 2: Epilepsy-/Toxo- (E-, T-) (n = 10), Group 3: Epilepsy-/Toxo+ (E-, T+) (n = 10), Group 4: Epilepsy+/Toxo+ (E+, T+) (n = 10). HMGB1, RAGE, TLR4, TLR1, TLR2, TLR3, IRAK1, IRAK2, IKBKB, IKBKG, BCL3, IL1 beta, IL10, 1 L8 and TNF alpha mRNA expression levels in the HMGB/RAGE/TLR4/NF-kappa B signalling pathway were determined by quantitative simultaneous PCR (qRT-PCR) after collecting blood samples from all patients in the groups. Statistical analysis was performed by one-way ANOVA followed by LSD post-hoc tests, and p < 0.05 was considered to denote statistical significance. The gene expression levels of HMGB1, TLR4, IL10, IL1B, IL8, and TLR2 were significantly higher in the G1 group than in the other groups (p < 0.05). In the G3 group, RAGE and BCL3 gene expression levels were significantly higher than in the other groups (p < 0.05). In the G4 group, however, IRAK2, IKBKB, and IKBKG gene expression levels were significantly higher than in the other groups (p < 0.05). HMGB1, TLR4, IRAK2, IKBKB, IL10, IL1B, IL1B, and IL8 in this signalling pathway are highly expressed in epilepsy patients in G1 and seizures occur with the stimulation of excitatory mechanisms by acting through this pathway. The signalling pathway in epilepsy may be activated by HMGB1, TLR4, and TLR2, which are considered to increase the level of proinflammatory cytokines. In T. gondii, this pathway is activated by RAGE and BCL3.
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    The Effects of Acute and Chronic Metformin Treatment on Penicillin Induced Epileptiform Activity in Rats
    (Galenos Publ House, 2022) Kilic, Umit; Demir, Serif; Beyazcicek, Ersin; Beyazcicek, Ozge; Soyturk, Hayriye
    Objective: The aim of this study is to investigate acute and chronic administered metformin on epileptiform activity induced by penicillin and antioxidant activity in rats. Methods: Eighty-four adult male Wistar albino rats were used in this study. The rats were divided into two large groups as acute and chronic groups, and later on each group was divided into different subgroups as control, sham, penicillin, metformin 100 mg/kg (Met_100), 200 mg/kg (Met_200) and only metformin 200 mg/kg (OMet_200) intraperitoneally. The substances were applied to the chronic groups for 21 days, while acute groups received them just before the initiation of epileptiform activity. In the present study, onset of first epileptiform activity, spike wave frequency and amplitude, and superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) parameters were evaluated. Results: No epileptiform activity was observed in the control, sham, and OMet_200 groups. When metformin doses of 100 mg/kg, 200 mg/kg were compared with the penicillin group in both acute and chronic groups, the onset of first epileptiform activity was prolonged, spike wave frequency and spike wave amplitude decreased significantly. SOD, CAT and GPx levels were found to be significantly different in the acute and chronic metformin groups compared to the penicillin group. Conclusion: In conclusion, this study shows that metformin can decrease epileptic seizures and increase the level of antioxidant enzymes and it can be used in the treatment of epilepsy in the future.
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    HMGB1 related pathways in epilepsy
    (Nova Science Publishers, Inc., 2022) Soyturk, Hayriye; Kilic, Umit; Onal, Cansu; Yildiz, Aysegül
    Epilepsy is one of the most common neurological illnesses, affecting an estimated 70 million individuals worldwide. A mechanistic approach to discovering crucial pathogenic brain abnormalities driving seizure onset, recurrence, and advancement is critical for generating novel and rational treatment methods that may modify or prevent disease progression. In this context, an increasing body of evidence suggests that neuroinflammation plays a role in drug-resistant epilepsies. The high mobility group box 1 (HMGB1) protein, a key regulator of neuroinflammation, has been associated with several neurological disorders, including epilepsy. Increased levels of HMGB1, one of the most prominent pro-inflammatory cytokines, have been linked to seizure length, recurrence, and epilepsy development. Therefore, HMGB1 has attracted a lot of attention and has been developed quickly. According to clinical and experimental data, HMGB1 isoforms may serve as neurobiological biomarkers for epileptogenesis and drug-resistant epilepsy. These novel findings suggest that the HMGB1 system could be targeted to prevent seizure generation and provide therapeutically relevant prognostic markers that can also predict a patient's response to therapy. This section will recap epileptogenesis theory and examine the relationships between epilepsy and neuroinflammatory pathways using experimental and clinical evidence. © 2023 by Nova Science Publishers, Inc. All rights reserved.
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    Investigation of the Effects of Acute and Chronic PTZ Model Epilepsy in Rats Exposed to Neonatal Hyperoxia on Bdnf, Ngf, Cyt c, Bax, and Bcl-2 Gene Expression Levels in the Brain
    (Galenos Publ House, 2023) Onal, Cansu; Kilic, Umit; Soyturk, Hayriye
    Objective: The aim of this study was to investigate the relationship between acute and chronic epilepsy that may occur in adulthood, gene expression levels, and the possible mechanism of neuronal loss in rats exposed to hyperoxia in the postnatal period. Methods: The study was started with 12 female rats (mother rat). Two main groups were formed: six control and six hyperoxia groups. At the end of the experiment, brain tissue samples were collected and Bdnf, Ngf, Cyt c, Bax, and Bcl-2 gene expressions were studied by quantitative polymerase chain reaction. Bax (Bcl-2 associated X-protein) and Cytochrome (Cyt) c gene expression levels were found to be significantly higher in the hyperoxia-epilepsy groups, especially in the male group, than in the other groups (p<0.05). Results: While the Ngf gene expression level increases significantly in females due to epilepsy, it is independent of hyperoxy (p<0.05). Bdnf gene expression levels were found to be affected by hyperoxia in both males and females (p<0.05). In our study, a significant increase in Bax and Cyt c gene expression levels was observed in the neonatal hyperoxia and epilepsy group. Conclusion: It is thought that this increase in gene expression levels molecularly supports neuronal loss, but the related pathways will be better clarified with further studies.
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