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作 者:丁未尧[1,2] 周凯 谢航 徐华容[1,2] 李彩蓉 蔡飞[1,2]
机构地区:[1]湖北科技学院糖尿病心脑血管病变湖北省重点实验室,湖北咸宁437100 [2]湖北科技学院药学院药理学教研室
出 处:《湖北科技学院学报(医学版)》2017年第5期372-374,共3页Journal of Hubei University of Science and Technology(Medical Sciences)
基 金:大学生创新创业项目(201410927001;201510927010);湖北省自然科学基金项目(2017CFB410)
摘 要:目的研究氧化苦参碱(OMT)对阿尔茨海默病(AD)大鼠认知功能障碍的作用及机制。方法取32只雄性SD大鼠分为四组,正常对照组给予生理盐水灌胃;STZ组给于大鼠侧脑室注射链脲佐菌素(STZ)制作AD学习记忆障碍模型后给于生理盐水灌胃;STZ+OMT组在建立AD模型后给予OMT灌胃;OMT组给予OMT灌胃。每组各8只,连续给药2周。通过Morris水迷宫检测大鼠的学习记忆情况;Elisa法测定海马组织炎症因子的变化。结果大鼠Morris水迷宫行为学实验发现STZ组大鼠记住原有平台所在位置的能力较差,经过OMT治疗后,大鼠在目标象限停留的时间有明显的增加(P<0.05)。STZ组大鼠海马组织细胞因子TNF-α和IL-6的含量明显升高(P<0.01),经过OMT给药后,TNF-α和IL-6的含量明显的下降(P<0.01)。结论OMT可改善STZ侧脑室注射所致大鼠学习记忆损害,该作用与抑制脑组织炎性反应有关。Objective To explore the effect and mechanism of oxymatrine on cognitive dysfunction in rats with Alzheimers disease. Methods 32 male SD rats were divided into four groups. The control group was given normal saline. The model of AD like learning and memory impairment was made by intracerebroventricular injection of streptozotocin (STZ). The STZ + OMT group was given orally with OMT after intracerebroventricu-lar injection of STZ. The OMT group was given intragastric administration of OMT. Each group had 8 rats, and they were given 2 weeks of continuous administration. The learning and memory ability of rats was detected by Morris water maze and the changes of inflammatory reaction in hippocampus were determined by Elisa test. Re-sults The Morris Morris water maze test showed that the ability of STZ treated rats to remember the location of the original platform was poor. After OMT treatment, the time of the rats staying in the target quadrant was sig- nificantly increased(T5 〈0. 05). The levels of TNF-a and IL-6 in hippocampus of STZ group were significantly increased (P 〈0.01) ,and the contents of TNF-a and IL-6 were significantly decreased after OMT administra-tion, (P 〈0. 01) . Conclusion Oxymatrine can improve the learning and memory impairment induced by intrac-erebroventricular injection of STZ in rats which may be related to the inhibition of inflammatory response in brain tissue.
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