本研究旨在探讨弓形虫病与该通路的关系,可能通过HMGB1/RAGE/TLR4/NF-κB信号通路作用于特发性癫痫患者的癫痫形成。在研究中,通过选择弓形虫IgG阳性和阴性的特发性癫痫患者和健康对照,形成四个不同的实验组。实验组如下:第1组:癫痫+/Toxo-(E+,T-)(n=10),第2组:癫痫-/弓形虫(E-,T-)(n=10),第3组:癫痫-/Toxo+(E-,T+)(n=10),第4组:癫痫+/Toxo+(E+,T+)(n=10)。HMGB1,RAGE,TLR4,TLR1,TLR2,TLR3,IRAK1,IRAK2,IKBKB,IKBKG,BCL3,IL1β,HMGB/RAGE/TLR4/NF-κB信号通路中的IL10、1L8和TNFαmRNA表达水平通过定量同时PCR(qRT-PCR)在收集各组中所有患者的血样后测定。通过单因素方差分析进行统计分析,然后进行LSD事后检验。并且p<0.05被认为表示统计学显著性。HMGB1、TLR4、IL10、IL1B、G1组的IL8、TLR2显著高于其他组(p<0.05)。在G3组中,RAGE和BCL3基因表达程度显著高于其他各组(p<0.05)。在G4组中,然而,IRAK2IKBKB,和IKBKG基因表达程度显著高于其他各组(p<0.05)。HMGB1,TLR4,IRAK2,IKBKB,IL10,IL1B,IL1B,该信号通路中的IL8在G1期癫痫患者中高表达,癫痫发作是通过该通路作用刺激兴奋性机制而发生的。癫痫中的信号通路可能被HMGB1、TLR4和TLR2激活,它们被认为增加了促炎细胞因子的水平。在T.Gondii,该途径被RAGE和BCL3激活。
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-κB 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, IL1β, IL10, 1 L8 and TNFα mRNA expression levels in the HMGB/RAGE/TLR4/NF-κB 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.