【摘要】 目的观察红景天对实验性老年痴呆大鼠认知功能的治疗作用。方法制作老年痴呆及红景天干预大鼠模型,Morris水迷宫检测大鼠模型学习记忆能力;免疫印迹法检测AKT、p-AKT、GSK-3β、p-GSK-3β、bcl-2及bax蛋白表达水平,电镜观察大鼠海马组织超微结构。结果造模后模型组、红景天组逃避潜伏期时间均长于对照组;治疗后逃模型组、红景天组避潜伏期时间均长于对照组,而红景天组短于模型组(P<0.05)。造模后模型组、红景天组目标象限停留时间均明显短于对照组(P<0.05);治疗后模型组、红景天组目标象限停留时间均短于对照组,而红景天组长于模型组(P<0.05)。p-GSK-3β蛋白红景组与模型组低于对照组,红景天组高于模型组;p-AKT蛋白红景天组高于对照组与模型组,模型组低于对照组(P<0.05)。bcl-2模型组低于对照组,红景天组高于对照组和模型组,(P<0.05);bax模型组高于对照组和红景天组(P<0.05)。结论红景天可改善实验性老年痴呆大鼠认知功能,其机制可能是通过PI3K/AKT/GSK3β通路上调抑制凋亡蛋白bcl-2、下调促凋亡蛋白bax实现的。更多还原

【Abstract】 Objective To study the therapeutic effects of Rhodosin on cognitive function in Alzheimer disease( AD) rats. Methods The AD rat models and Rhodosin intervention models were established. Learning and memory abilities of rats were tested by the Morris water maze. The protein expressions of AKT,p-AKT,GSK-3β,P-GSK-3β,bcl-2 and bax were examined via Western blotting.And the ultrastructure of hippocampus neurons was determined by transmission electron microscopy.Results After modeling,the latent period of the model group and Rhodosin group was prolonged than that in the control group. After treatment,the latent period of the model group and Rhodosin group was prolonged than that in the control group. The Rhodosin group was shorter than the model group( P <0. 05). After modeling,the stay time of the target quadrant in model group and Rhodosin group was significantly shorter than the control group,the difference was statistically significant( P < 0. 05). After treatment,the stay time of the target quadrant in model group and Rhodosin group was also shorter than the control group,but the Rhodosin group was longer than the model group( P < 0. 05). The protein expressions of p-GSK-3β in the model group and Rhodosin group was lower than that in the controlgroup,Rhodosin group higher than model group. The protein expressions of p-AKT in Rhodosin group was higher than control group and model group,model group lower than control group( P < 0. 05). The protein expressions of bcl-2 in model group lower than control group,Rhodosin group was higher than control group and model group( P < 0. 05). The bax protein expressions in model group was high than control group and Rhodosin group( P < 0. 05). Conclusion Rhodosin could improve cognitive function in AD rats. Its mechanisms may be through up-regulating anti-apoptotic protein bcl-2 and down-regulating pro-apoptotic protein bax via the PI3 K / AKT / GSK3β pathway.更多还原