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目的观察外伤性癫痫(post traumatic epilepsy,PTE)大鼠模型海马CA3区巢蛋白(nestin)、核因子-kB(NF-kB)及胶质纤维酸性蛋白(GFAP)的动态表达,探讨PTE可能的发病机制。方法健康成年雄性SD大鼠采用随机数字表法分为正常对照组(A,n=6)和癫痫模型组(B,n=20)。A组不做任何处理,B组注射1μmol FeCl2于右额叶运动皮层。观察行为学、脑电图,在不同时间点取脑,分别行抗NF-kB、Nestin及GFAP酶标免疫组织化学染色,对海马CA3区行病理学观察。结果B组大鼠在注射FeCl2后制模成功并存活15只。与A组比较,B组在1d海马CA3区Nestin表达逐渐增加,7d时表达最强,差异均有统计学意义(P<0.05),14d时降低;NF-kB在1d时大量表达,7d后减少,14d明显减少;GFAP在7d表达增强,14d时最多,差异均有统计学意义(P<0.05)。结论在PTE后Nestin表达逐渐增多,神经元及胶质细胞NF-kB表达高峰出现早。通过氧化应激反应,诱导海马神经前体细胞的增殖分化,或者诱导神经胶质细胞自身增殖/增生,可能在晚期PTE的发病机制中起重要作用。
Objective To observe the dynamic expression of nestin, nuclear factor-kB (NF-kB) and glial fibrillary acidic protein (GFAP) in hippocampal CA3 area of rat model of traumatic epilepsy (PTE) Pathogenesis. Methods Healthy male Sprague-Dawley rats were randomly divided into normal control group (A, n = 6) and epilepsy model group (B, n = 20). Group A did not do any treatment, group B injected 1μmol FeCl2 in the right frontal cortex. The behavior and EEG were observed. The brain was taken at different time points. The pathological changes of hippocampal CA3 area were observed by immunohistochemical staining of NF-κB, Nestin and GFAP respectively. Results After injection of FeCl2, rats in group B succeeded in modeling and survived 15. Compared with group A, nestin expression in CA3 area of group B on day 1 increased gradually and reached its peak on day 7 (P <0.05), and decreased on the 14th day. NF-kB was abundantly expressed on day 1, and after 7 days (P <0.05). GFAP increased on the 7th day and reached the maximum on the 14th day, the difference was statistically significant (P <0.05). Conclusion The expression of Nestin increased gradually after PTE, and the expression peak of NF-κB in neurons and glial cells appeared earlier. It may play an important role in the pathogenesis of advanced PTE by inducing the proliferation and differentiation of hippocampus neural precursor cells or inducing glial cell proliferation / proliferation through oxidative stress.