论文部分内容阅读
目的观察β-蜕皮甾酮(20-hydroxyecdysone)对小鼠癫痫持续状态后海马神经元凋亡及凋亡相关基因的影响。方法将30只CD-1小鼠随机分成正常组、造模组、β-蜕皮甾酮治疗组。用锂-匹罗卡品腹腔注射法诱导小鼠癫痫持续状态,造模成功后72h,采用尼氏染色观察各组小鼠海马区神经元数目和形态的变化,免疫组化法和Westernblot法检测各组神经元凋亡及凋亡相关基因Bcl-2,Bax的表达。结果模型组小鼠CA1区部分细胞肿胀,锥体细胞排列紊乱,细胞形态不规则,药物治疗组较模型组细胞数目增多,细胞排列有所改善。免疫组化和Westernblot结果可见细胞凋亡因子Bax表达模型组高于正常对照组,药物治疗组低于模型组;抑制细胞凋亡因子Bcl-2表达模型组高于正常对照组,药物治疗组高于模型组。结论β-蜕皮甾酮(20-HE)可能通过降低Bax,提高Bcl-2蛋白的表达,减轻癫痫发生后对大脑的损害。
Objective To investigate the effects of β-ecdysterone on apoptosis and apoptosis-related genes in hippocampal neurons after status epilepticus in mice. Methods Thirty CD-1 mice were randomly divided into normal group, model group and β-ecdysterone treatment group. The status of epilepsy in mice was induced by intraperitoneal injection of lithium-pilocarone. The number and morphology of neurons in hippocampus of each group were observed by Nissl’s staining 72 hours after the model was established. Immunohistochemistry and Western blotting Apoptosis and expression of Bcl-2 and Bax in neurons of each group. Results In the model group, some cells in the CA1 region were swollen, the pyramidal cells were disordered and the cells were irregular in shape. The number of cells in the drug-treated group increased compared with that in the model group, and the cell arrangement improved. The results of immunohistochemistry and Western blot showed that the expression of Bcl-2 in the model group was higher than that in the normal control group, and that in the drug-treated group was lower than that in the model group. The expression of Bcl-2 was higher in the model group than in the normal control group In the model group. Conclusion β-ecdysterone (20-HE) may reduce brain damage after epilepsy by decreasing Bax and increasing Bcl-2 protein expression.