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目的探讨环氧合酶-2抑制药塞来昔布对慢性颞叶癫癎大鼠海马核因子-κBp65和P-糖蛋白表达的影响,以及核因子-κBp65和P-糖蛋白与颞叶癫癎发病机制的关系,以为环氧合酶-2抑制药用于抗癫癎药物辅助治疗提供实验依据。方法采用大鼠海马CA3区微量注射海人酸的方法制备颞叶癫癎动物模型,免疫组织化学染色和Western blotting法观察塞来昔布治疗后大鼠海马核因子-κBp65和P-糖蛋白表达变化。结果与对照组相比较,颞叶癫癎大鼠海马核因子-κBp65、P-糖蛋白表达水平,以及核因子-κBp65核移位现象明显增加(均P<0.05);经塞来昔布治疗后,海马组织中核因子-κBp65、P-糖蛋白表达水平及核因子-κBp65核移位现象显著改善,与模型组比较差异有统计学意义(均P<0.05)。结论核因子-κBp65和P-糖蛋白在颞叶癫癎慢性期表达上调、核因子-κBp65核移位现象增加,有可能是难治性癫癎发生与发展的分子生物学机制之一。环氧合酶-2抑制药塞来昔布通过降低慢性颞叶癫癎大鼠海马CA3区核因子-κBp65和P-糖蛋白表达水平,抑制核因子-κBp65核移位,最终降低炎性反应,逆转多药耐药而发挥抗癫癎作用。
Objective To investigate the effect of cyclooxygenase-2 inhibitor celecoxib on the expression of NF-κBp65 and P-glycoprotein in the hippocampus of chronic temporal lobe epilepsy rats, and the relationship between NF-κBp65, P-glycoprotein and temporal lobe epilepsy癎 pathogenesis of the relationship that the cyclooxygenase-2 inhibitors for the treatment of anti-epileptic drugs to provide experimental evidence. Methods The model of temporal lobe epilepsy was prepared by microinjection of kainate into hippocampal CA3 area of rat hippocampus. The expression of nuclear factor-κBp65 and P-glycoprotein in hippocampus of rats after treatment with celecoxib was observed by immunohistochemical staining and Western blotting Variety. Results Compared with the control group, the expression of nuclear factor-κBp65, P-glycoprotein and the nuclear translocation of nuclear factor-κBp65 in the temporal lobe epileptic rats were significantly increased (all P <0.05); after celecoxib treatment The expression of nuclear factor-κBp65, P-glycoprotein and nuclear factor-κBp65 nuclear translocation in hippocampus were significantly improved, which were significantly different from the model group (all P <0.05). Conclusion The expressions of nuclear factor-κBp65 and P-glycoprotein in the chronic phase of temporal lobe epilepsy are up-regulated, and nuclear translocation of nuclear factor-κBp65 is increased, which may be one of the molecular biological mechanisms of the occurrence and development of intractable epilepsy. Cyclooxygenase-2 inhibitor Celecoxib inhibits the nuclear translocation of nuclear factor-κBp65 by decreasing the levels of nuclear factor-κBp65 and P-glycoprotein in hippocampal CA3 region of rats with chronic temporal lobe epilepsy and eventually decreases the inflammatory response , Reverse multidrug resistance and exert antiepileptic effect.