氨基胍对癫痫大鼠海马区bcl-2、bax蛋白表达的影响

Study on effect of aminoguanidine on expression of hippocampal Bcl-2 and Bax protein in epileptic rat models

目的探讨氨基胍对癫痫大鼠海马区bcl-2、bax蛋白表达的影响。方法 32只SD大鼠随机分为4组:空白对照组(NS+NS组),模型组(NS+KA组),氨基胍预处理组(AG+KA组)和单纯氨基胍组(AG+NS组),每组8只。4组大鼠造模后存活24 h、48 h,免疫组织化学法显示bcl-2、bax的蛋白表达情况。结果 bcl-2的免疫反应在NS组和AG组最强,AG+KA组次之,KA组最弱;bax的免疫反应在KA组最强,AG+KA组次之,NS组和AG组最弱。结论氨基胍预处理癫痫模型大鼠可以使bcl-2的表达增加、bax的表达降低。

Objective To explore the regulatory effect of aminoguanidine on expression of hippocampal Bcl - 2 and Bax protein in epilep- tic rat models. Methods A total of 32 SD rats were divided into 4 groups： normal saline （NS） control group, kainic acid （KA） group, amin- oguanidine （AG） pretreatment plus KA （AG ＋ KA） group, and AG group. Immunohistochemical method was applied in detection of levels of Bcl -2 and Bax protein in rathippocampus by staining for 24h and 48h after modeling. Results The protein expression of Bcl -2 was the strongest in NS and AG groups, followed by AG ＋ KA group, and KA group was the weakest one. The protein expression of Bax was the strongest in KA group, followed by AG ＋ KA group, and NS and AG groups were the weakest groups. Conclusion KA - induced epilepsy can down - regulate the expression of Bcl - 2 protein and up - regulate the expression of Bax protein, while AG pretreatment can reduce the NO levels, thus it may an- tagonize this effect.