简介：Inthisstudy,wesoughttoelucidatetheeffectsofmelatoninonlearningandmemoryaswellasapoptosisandexpressionoftheBaxorBcl-2proteinsinthesubgranularzoneofthedentategyrusinpinealectomizedrats.UsingtheMorriswatermazeandtheolfactorymemorytests,wefoundthattheaverageescapelatencyinpinealectomizedratswasclearlyincreasedcomparedwithsham-operatedrats.Moreover,theaverageescapelatencyinthemelatonin-treatedandpinealectomizedratswaslongerthanthatinthesham-operatedratsandshorterthanthatinthepinealectomizedanduntreatedrats.Immunohistochemistryandterminal-deoxynucleoitidyltransferasemediatednickendlabeling(TUNEL)showedthattherewerefewerBaximmunoreactivecellsandTUNEL-positive(apoptotic)cellsbutmoreBcl-2immunoreactivecellsinthemelatonin-treatedratscomparedwiththepinealectomizedrats.Thesham-operatedratsshowednumbersofthesecellssimilartothemelatonin-treatedrats.TheseexperimentalfindingsdemonstratethatmelatonintreatmentmayreduceabnormalapoptosisbypromotinggeneexpressionofBaxandsuppressinggeneexpressionofBcl-2inthesubgranularzoneofthedentategyrusinpinealectomizedrats.Theseeffectsappeartoresultintheinhibitionofcellularapoptosisandtheimprovementofspatiallearningandmemoryinpinealectomizedrats.

简介：目的研究杏仁核注射β-淀粉样肽（Aβ25-35）所致阿尔茨海默病（AD）模型大鼠脑内Aβ1-40、Bax的表达变化，以及葛根素（Pue）的影响。方法将30只SD大鼠随机分为假手术组、AD模型组和Pue治疗组，以Aβ25-35。右侧杏仁核注射制备大鼠AD模型，用Y-型迷宫检测大鼠学习记忆能力，用免疫组织化学方法检测大脑皮层与海马组织Aβ1-40。和Bax的表达。结果假手术组脑内有Aβ1-40、Bax的少量表达，两者均以皮层内为多，海马组织内少；AD模型组大鼠皮层和海马组织Aβ1-40与Bax的表达增加．较假手术组大鼠有显著性差异．P〈0．01；Pue能改善AD模型组大鼠的学习记忆能力，Pue治疗组大鼠皮层和海马组织Aβ1-40、Bax表达减少，与AD模型组比较有显著性差异，P〈0．05。结论Pue可能通过下调脑组织Aβ1-40和Bax表达，抑制β-淀粉样肽的神经毒性，减轻脑皮层和海马神经元凋亡．具有神经保护及抗痴呆作用。

简介：目的探讨氧增强放疗对胶质瘤凋亡相关基因Bcl-2、Bax影响的差异.方法建立大鼠胶质瘤动物模型,治疗组10只,高压氧处理后放疗;对照组10只,常规放疗.免疫组化检测凋亡相关基因Bcl-2、Bax的表达.结果治疗组Bcl-2表达明显低于对照组,组间差异有显著性（P＜0.05）;治疗组Bax的表达明显高于对照组,组间差异有显著性（P＜0.05）.结论氧增强放疗可以更有效地抑制Bcl-2、增加Bax的表达.