甲硫氨酸维B_1对创伤性癫痫大鼠的治疗机制研究

The therapeutic mechanism after methionine and vitamin B_1 treatment for posttraumatic epilepsy rats

目的探讨甲硫氨酸维B_1(MVB_1)对创伤性癫痫(PTE)的治疗机制。方法将15只雄性SD大鼠随机分为假手术组、癫痫组和癫痫MVB1治疗组,Morris水迷宫方法观察各组大鼠学习和记忆行为变化,检测各组大鼠血清和海马组织中超氧化物歧化酶(SOD)、丙二醛(MDA)和还原性谷胱甘肽(GSH)浓度变化。结果癫痫组大鼠5d的逃避潜伏期显著延长,站台穿越次数显著降低,目标象限时间显著缩短,血清及海马组织SOD和GSH水平显著降低,MDA水平显著增加。癫痫大鼠MVB1处理后,5d的逃避潜伏期均显著缩短,站台穿越次数显著增加,目标象限时间显著延长,血清及海马组织SOD和GSH水平显著增加,MDA水平显著降低。结论 MVB1可改善PTE大鼠的学习记忆功能,可通过提高SOD和GSH浓度,降低MDA浓度来抑制脂质过氧化和减轻自由基损伤,为MVB1临床治疗癫痫提供了新的理论依据。

Objective To explore the therapeutic mechanism after methionine and vitamin B1（MVB1） treatment for posttraumatic epilepsy rats. Methods A total of 15 male SD rats were divided into sham-operated group（Sham）, epilepsia group（EP）and epilepsia plus MVB1 treatment group（EP＋MVB1）. Morris water maze was used for observe the learning and memory of rats. The levels of superoxide dismutase（SOD）, malondialdehyde（MDA） and reduced glutathione（GSH）concentration in serum and hippocampus tissue were measured. Results The escape latency of 5 days of the EP group rats significantly prolonged, the platform through the number decreased significantly and the target quadrant time was significantly shortened, the levels of SOD and GSH in serum and hippocampus were significantly decreased as well as MDA level increased significantly compared to sham-operated group rats. The escape latency of 5 days significantly shortened, the platform through the number increased significantly and the target quadrant time was significantly prolonged, the levels of SOD and GSH in serum and hippocampus were significantly increased as well as MDA level decreased significantly in EP＋MVB1 rats compared to EP rats. Conclusion MVB1 can improve learning and memory function of posttraumatic epilepsy rats as well as MVB1 treatment could improved the level of SOD and GSH and reduced the level of MDA, and then inhibit lipid peroxidation and mitigate free radical damage. The results provided the experimental basis.