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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.
  • Küçük Resim
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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.