摘要： 目的 通过观察普瑞巴林对匹罗卡品慢性癫大鼠海马区Bcl?2 和Bax 表达的影响，探讨普瑞巴林治疗癫的药理学机制及对大鼠海马神经元的抗凋亡作用。方法 采用氯化锂-匹罗卡品化学诱导方法建立慢性颞叶癫模型。经腹腔注射普瑞巴林40 mg/（kg·d）连续治疗3 周，免疫组织化学染色和Western blotting 法检测不同处理组大鼠海马区Bcl-2 和Bax表达变化。结果 与生理盐水对照组比较，模型组大鼠海马区Bcl-2 和Bax 表达水平显著升高（均P = 0.000）；与模型组比较，普瑞巴林治疗组大鼠海马区Bcl-2 表达水平升高、Bax 表达水平降低，组间差异具有统计学意义（均P = 0.000）。结论 新型抗癫药物普瑞巴林可通过降低慢性颞叶癫大鼠海马区Bax 表达、上调Bcl-2 表达而抑制细胞凋亡，发挥神经元保护作用。

关键词: 癫, 颞叶, 细胞凋亡, 基因, bcl-2, bcl-2 相关X 蛋白质, 抗惊厥药, 免疫组织化学, 印迹法, 蛋白质

Abstract: Objective To observe the effect of pregabalin on the expression of Bcl-2 and Bax in hippocampus of chronic epileptic rats induced by pilocarpine, to explore the anti-epileptic pharmacology mechanism of pregabalin, and its anti-apoptotic effect on hippocampal neurons of rats. Methods The model of chronic temporal lobe epileptic rats induced by lithium-pilocarpine was established, then the rats in pregabalin treatment group received intraperitoneal injection of pregabalin (40 mg/kg) once daily for three weeks. The expression of Bcl-2 and Bax in hippocampus of all rats was detected by immunohistochemical technique and Western blotting. Results Compared with normal saline group rats, the expression of Bcl-2 and Bax in hippocampus of rats with chronic temporal lobe epilepsy was significantly increased (P = 0.000, for all). Pregabalin can down-regulate the expression of Bax and up-regulate the expression of Bcl-2 in hippocampus of rats compared to model group rats (P = 0.000, for all). Conclusion Pregabalin may have the effects of inhibiting cell apoptosis and protecting neurons through lowing Bax level and increasing Bcl-2 level in hippocampus of chronic temporal lobe epileptic rats.

Key words: Epilepsy, temporal lobe, Apoptosis, Genes, bcl-2, bcl-2-associated X protein, Anticonvulsants, Immunohistochemistry, Blotting, western