摘要
目的检测慢性脑缺血后水通道蛋白9(AQP9)的表达及其影响。方法将大鼠随机分为对照组和慢性脑缺血1、3和6月组,每组各20只。用双侧颈总动脉结扎法(2-vo法)建立大鼠慢性脑缺血模型,水迷宫实验检测大鼠的学习记忆能力,干湿重法检测脑含水量,HE染色观察脑组织缺血后形态学,吸光度法检测脑组织乳酸含量,免疫荧光和免疫印迹测定AQP9的表达。结果与对照组相比,慢性脑缺血组大鼠的学习记忆明显下降(P<0.05),脑含水量无明显变化,慢性脑缺血各组的脑乳酸含量较对照组上调(P<0.05);慢性脑缺血组脑组织胶质细胞增生,神经元凋亡坏死;与对照组相比,慢性脑缺血各组AQP9的表达上调(P<0.05)。结论慢性脑缺血后脑组织中AQP9表达上调,可能与缺血后能量底物的转运有关。
Objective To investigate the expression of aquaporin 9（ AQP9） and its influence on chronic cerebral ischemia. Methods Rats were randomly divided into sham operation group and chronic cerebral ischemia 1,3 and6 months groups. Chronic cerebral ischemia model was developed by ligation of bilateral common carotid artery（ 2-vo）. The animals were sacrificed after chronic cerebral ischemia. The ability of learning and memory of rats was measured by morris water maze test. Brain water content（ BWC） was measured by wet-dry ratio. HE staining was used to observe the morphological changes after cerebral ischemia. The contents of lactic acid in brain were measured by absorption spectrophotometry. Immunofluorescence and Western blot were used to test the expression of AQP9 in brain. Results Compared with the sham operation group,the ability of learning and memory of rats in all chronic cerebral ischemia groups decreased distinctly. Brain water content did not change in all groups of chronic cerebral ischemia. Proliferation of glial cells and neurons apoptosis were found in all chronic cerebral ischemiagroups detected by HE staining. The contents of lactic acid in brain increased in all chronic cerebral ischemia groups（ P〈0. 05）. The expression of AQP9 increased in all chronic cerebral ischemia groups as shown by immunofluorescence and Western blotting（ P〈0. 05）. Conclusions The expression of AQP9 increased after chronic cerebral ischemia,which may contribute to transportation of energy substrate after ischemia.
出处
《基础医学与临床》
CSCD
2016年第6期747-751,共5页
Basic and Clinical Medicine
基金
国家自然科学基金(81000566)
重庆医科大学基础医学院苗圃基金(JC201506)
重庆医科大学大学生科学研究与创新实验(201502)
重庆市自然科学基金(CSTC2011JJA10093
CSTC2015JJA10383)
高等学校博士学科点专项科研基金(201005503120009)
