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目的:探讨核转录因子(NF-κB)p65在癫癇大鼠海马结构中的激活及其意义,并观察钙调蛋白抑制剂W-7的干预作用。方法:健康SD大鼠58只,随机分为5组,对照组、戊四唑(PTZ)组和三个剂量的W-7组,通过行为学观察探讨W-7的抗癫癇作用,应用免疫组织化学方法和免疫印迹方法检测海马组织NF-κBp65蛋白表达的变化。结果:同对照组比较,3个剂量的W-7大鼠发作程度明显减轻,差异有显著性(P<0.01);免疫组织化学染色和免疫印记实验显示,PTZ组NF-κBp65蛋白表达明显增强(P<0.01),3个剂量的W-7组表达明显减弱,其差异均具有显著性意义(P<0.05,P<0.01)。结论:PTZ导致癫癇大鼠脑组织中NF-κBp65蛋白表达增高。W-7对PTZ诱导的癫癇大鼠具有保护作用,其作用是通过抑制NF-κBp65的蛋白表达实现的。
Objective: To investigate the activation and significance of NF-κB p65 in the hippocampal formation of epileptic rats and to observe the intervention effect of calmodulin inhibitor W-7. Methods: Fifty-eight healthy SD rats were randomly divided into five groups: control group, PTZ group and three doses of W-7 group. The anti-epileptic effects of W-7 were observed through behavioral observation. The changes of NF-κBp65 protein expression in hippocampus were detected by histochemistry and Western blotting. Results: Compared with the control group, the W-7 rats in three doses significantly reduced the degree of attack (P <0.01), and the expression of NF-κBp65 protein in PTZ group was significantly increased by immunohistochemistry and immunoblotting (P <0.01). The expression of W-7 in three doses was significantly weakened, the difference was significant (P <0.05, P <0.01). Conclusion: PTZ can induce the expression of NF-κBp65 in brain tissue of epileptic rats. W-7 has a protective effect on PTZ-induced epileptic rats by inhibiting the protein expression of NF-κBp65.