| Background: Pediatric epilepsy is a nervous syndrome with complicated etiopathogenesis as well as recurrent, which is a debilitating disease and ranking it first amongst brain chronic disease in children. It is an abnormal brain neurons synchronized discharge caused by various reasons resulting in the central nervous system dysfunction. Pediatric epilepsy not only affects children’s physical and mental health but also brings heavy burden to family and society.75 percent of Drug non-responsive epilepsy, which need surgical treatment to remove epileptogenic focuses accounts for about 30 percent of all epilepsy, is focal cortical dysplasia. Focal cortical dysplasia, which is caused by the normal procedures such as neuron proliferation, migration and differentiation interferencein in the early embryo, is one of the subtypes of cortical dysplasia. Its typical pathological change is abnormal cortical layers and/or aliens, ectopic neurons. Focal cortical dysplasia is one of the most common pathological type in children with intractable epilepsy. According to the pathology it can be divided into the simplex(FCD type I and type FCDII) and combined type(FCDIII), and each is divided into different subtypes, among of them FCDIII have three subtypes, FCDIIIa, FCD Ⅲ b, FCDⅢc and FCDⅢd.Nuclear factor-kappa B(NF-κB) specific binding with enhancer κB sequence of κ light chain is a kind of nucleoprotein and one of key transcription factor. It is the upstream regulating factor of many cytokine and has wide biologic activity.P65?P50 heterodimer, which is regulated by IΚBa and IΚBB, produces a marked effect on central nervous system. Many ectospike can activate NF-κB to change DNA conformation, priming or reinforce target gene transcription and regulate transcription of some genes such as cytokine, adhesion factor, enzyme and chemotatic factor. Lots of studies found NF-κB as transcription factor participated in acute inflammation in epilepsy. It regulate not only expression of cytokines,but also chemotatic factor such as IL-8. Therefore, NF-κB play an important role in inflammatory reaction through regulating above-mentioned factors. Another studies indicated NF-κB was correlated with neuron plasticity and delivered long termpotentiation through hippocampus synapse to regulate structure and function change. Lots of empirical studies indicated NF-κB nucelus shifting was correlated closely with production, development and maintenance of epilepsy. But there is not report about whether NF-κB participate in pathology of FCDIIIa.Objectives: FCDIIIa is one of the most common pathological type in children with intractable epilepsy and its pathogenesis is not clear. At present some studies find NF-κB is related with epilepsyand the mechanism may be mediating inflammatory reaction. Reseaching the expression of NF-κBP65 in FCDIIIa is to explore the function of NF-κBP65 in pathogenesis of FCDIIIa.Methods: We selected children with intractable epilepsy who received surgical treatment in neurosurgery department of Hebei people’s hospital covering the period between October 2011 and April2013. We selected cortex specimens which were epileptogenic focusfrom 26 patients with FCD IIIa as the experimental group and normalcortex specimens which were from 5 autopsy specimens in department of pathology as the control group. We compared the differences of NF-κBP65 expression which was detected by immunohistochemical staining and Western Blot method between in the brain of the patients with FCD IIIa and in normal brain. The experimental data was analyzed by SPSS 13.0 statistical software.Results: In the experimental group, male 16 cases, female 10 cases, age from 2.5 to 14.0 years, the average age(8.81±2.98)years; Onset age from 0.5 to 7.0 years, the average age(4.31±1.84)years; and the duration from 2 to 7 years, the average duration(4.67±1.22)years. In the control group, 3 cases of male and 2 cases of female, age from 4.0 to 12 years, the average age(7.80±1.23)years. The results of immunohistochemical showed that expression of NF-kappa BP65 was significantly increased in the patients with FCD IIIa(28.95± 5.103) that that In the control group(7.20 ± 2.280). The difference between two groups was statistically significant(t = 9.186,P< 0.05). The protein levels of NF-κBP65was detected by western blot,the results showed that the espression of NF-κBP65 was higher in the cortex of children with FCDIIIa(49.2± 9.88)than that in the control group(24.5 ± 6.72).The difference between the two groups was statistically significant(t = 6.534,P< 0.05).Conclusions: The NF-κB(P65) in children with FCDIIIa expression is significantly higher than control group in the cerebral cortex, illustrate the NF-κB may be involved in the formation process of FCDIIIa. The NF-κB(P65) may be a mechanism is activated, the activation of the NF-κB may the mediated inflammatory reactions involved in the formation of a FCDIIIa pathological changes. |
