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作 者:李娟[1] 饶维[1] 吴颜艳[2] 荔志云[3] 马义辉[3] LI Juan RAO Wei WU Yanyan LI Zhiyun MA Yihui(Institute of Neurosurgery , Xijing Hospital, Fourth Military Medical U- niversity, Xi' an 710032, China The Department of Cardiology, Lanzhou General Hospital, Lan Zhou Command, Lanzhou, 730050, China The Department of Neurosurgery, Lanzhou General Hospital, Lan Zhou Command, Lanzhou, 730050, China)
机构地区:[1]第四军医大学西京医院神经外科,陕西西安710032 [2]兰州军区兰州总医院心脏内科,甘肃兰州730050 [3]兰州军区兰州总医院神经外科,甘肃兰州730050
出 处:《国际神经病学神经外科学杂志》2017年第2期171-175,共5页Journal of International Neurology and Neurosurgery
基 金:国家自然科学青年科学基金项目81401020
摘 要:目的探讨创伤性脑损伤后小鼠皮层和海马Wnt3a和β-Catenin的表达及其意义。方法在小鼠创伤性脑损伤模型基础上,采用免疫印迹法和免疫组织化学法检测创伤性脑损伤后Wnt3a和β-Catenin的蛋白变化。结果 Wnt3a和β-Catenin在对照组的脑组织中表达较低。创伤性脑损伤后1 h,皮层和海马区β-Catenin和Wnt3 a的含量开始增加。与对照组相比,伤后6h和第7天,β-Catenin和Wnt3a蛋白表达显著增加(P<0.05)。免疫荧光染色结果显示,脑损伤24 h后,β-Catenin和Wnt3a在小鼠皮层和海马表达量均增加。结论小鼠创伤性脑损伤后早期和恢复期,Wnt3a和β-Catenin的蛋白水平在皮层和海马显著增高,这提示Wnt3a和β-Catenin可能在创伤性脑损伤的病理生理机制中发挥着重要的作用。Objective To investigate the expression of Wnt3a and β-catenin in the cortex and the hippocampus after traumatic brain injury in mice and its clinical significance.Methods A mouse model of traumatic brain injury was established,and Western blotting and immunohistochemistry were used to measure the changes in the protein expression of Wnt3a and β-catenin after traumatic brain injury.Results The control group had low expression of Wnt3a and β-catenin in brain tissue.At 1 hour after traumatic brain injury,the content of β-catenin and Wnt3a in the cortex and the hippocampus started to increase.At 6 hours and 7 days after traumatic brain injury,the traumatic group had significant increases in the protein expression of β-catenin and Wnt3a (P 〈 0.05).Immunofluorescent staining showed that at 24 hours after brain injury,there were increases in the expression of β-catenin and Wnt3a in the cortex and the hippocampus.Conclusions The protein expression of Wnt3a and β-catenin increases significantly in the early stage and recovery stage after traumatic brain injury,suggesting that Wnt3a and β-catenin may play important roles in the pathophysiological mechanism of traumatic brain injury.
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