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目的探讨戊四氮(PTZ)所致大鼠严重惊厥发作模型中核因子κB(NFκB)活化与神经细胞凋亡的关系。方法42只大鼠随机分为7组,即对照组、致惊后3h、6h、12h、24h、48h和吡咯啉烷二硫代氨基甲酸盐(PDTC)+PTZ组。免疫组织化学法检测海马CA1区NFκB亚基p65核移位;TUNEL和流式细胞仪检测海马细胞凋亡。结果流式细胞仪和TUNEL法显示惊厥发作后有细胞凋亡的发生,24h达高峰,与对照组相比分别为(12.54±4.99)%vs(2.24±0.57)%和(61.62±4.99)个/gcsvs(3.35±0.89)个/gcs,P均<0.001;对照组大鼠海马未见p65核移位细胞,而致惊后p65核移位细胞显著上调,24h达高峰(32.30±4.71)个/gcs。PDTC预处理组与致惊24h组相比p65核移位及细胞凋亡明显减少。结论NFκB活化在严重惊厥发作所致的细胞凋亡发生中发挥重要作用;PDTC可通过抑制NFκB的表达而减少惊厥后的细胞凋亡。
Objective To investigate the relationship between activation of nuclear factor κB (NFκB) and apoptosis of nerve cells in rats with severe seizures induced by pentylenetetrazol (PTZ). Methods Forty-two rats were randomly divided into 7 groups: control group, 3h, 6h, 12h, 24h, 48h and PDTC + PTZ group. The nuclear translocation of NFκB subunit p65 in hippocampal CA1 region was detected by immunohistochemistry. The apoptosis of hippocampal cells was detected by TUNEL and flow cytometry. Results Flow cytometry and TUNEL showed that apoptosis occurred after convulsion seizure and peaked at 24h, which were (12.54 ± 4.99)% vs (2.24 ± 0.57)% and (61.62 ± 4.99) / gcsvs (3.35 ± 0.89) / gcs, P <0.001. There was no p65 nuclear translocation in the hippocampus of rats in the control group, while the nuclear translocation of p65 was significantly up-regulated in the control group (32.30 ± 4.71) / gcs. The p65 nuclear translocation and apoptosis in PDTC pretreatment group were significantly decreased compared with those in 24h group. Conclusion NFκB activation plays an important role in the apoptosis of seizures induced by severe seizures. PDTC can reduce the apoptosis after seizures by inhibiting the expression of NFκB.