深低温停循环大鼠大脑缺氧诱导因子-1α和信号转导分子2表达情况  

Expressions of hypoxia-inducible factor-1 alpha and Smad2 in the brain of rats with deep hypothermic circulatory arrest

作　　者：朱耀斌[1] 李志强[2] 范祥明[1] 刘东海[3] 张伟华[3] 廖秋明[4] 杨尧[1] 李刚[1] 刘扬[1] 续玉林[1] 张晶[1] 乔晨晖[3] 

机构地区：[1]首都医科大学附属北京安贞医院小儿心脏中心,北京100029 [2]首都医科大学附属北京儿童医院小儿心脏中心,北京100037 [3]郑州大学第一附属医院心外科,郑州450052 [4]瑞典隆德大学医院心胸外科,隆德SE-22185

出　　处：《中华实用诊断与治疗杂志》2016年第12期1162-1165,共4页Journal of Chinese Practical Diagnosis and Therapy

基　　金：国家自然科学基金(81371443);国家自然科学基金(81400305);北京市自然科学基金(7122056);北京市自然科学基金(7142049);北京市自然科学基金(7142137);北京市自然科学基金(7152045);首都医科大学基础-临床科研合作基金(13JL26);北京市优秀人才培养资助(2014000021469G233);北京市卫生局高层次人才培养资助(2014-3-043);北京市卫生局高层次人才培养资助(2015-3-048);北京市卫生局高层次人才培养资助(2015-3-051);北京市属医院科研培育项目(PX2016046)

摘　　要：目的探讨深低温停循环大鼠大脑缺氧诱导因子1α（hypoxia-inducible factor-1alpha,HIF-1α）和信号转导分子2（signal transduction molecule 2,Smad2）的表达情况,及HIF-1α和Smad2在深低温脑保护中的作用。方法 39只大鼠随机分为深低温停循环组、常温停循环组和常温不停循环组,每组各13只。深低温停循环组在肛温〈20℃下循环10min停循环10min,常温停循环组在肛温36.5-37.0℃循环10min停循环10min,常温不停循环组大鼠在肛温36.5-37.0℃体外循环20min。观察3组大鼠大脑脑组织组织病理变化,采用免疫组织化学法检测大鼠脑组织HIF-1α和Smad2蛋白表达情况。结果常温停循环组大鼠大脑少量神经元肿胀、神经元变性、胶质细胞增生、炎细胞浸润;深低温停循环组和常温不停循环组大鼠大脑神经细胞的数量和形态均正常,无明显病理学改变;深低温停循环组大鼠脑组织中HIF-1α和Smad2呈高水平表达,常温停循环组大鼠脑组织中HIF-1α和Smad2呈中等水平表达,常温不停循环组大鼠脑组织中HIF-1α和Smad2仅少量表达;深低温停循环组大鼠脑组织HIF-1α和Smad2蛋白平均灰度值（101.32±9.23、104.36±7.12）明显低于常温停循环组（123.35±7.26、113.42±7.33）和常温不停循环组（148.14±5.47、124.75±6.36）（P〈0.05）,常温停循环组低于常温不停循环组（P〈0.05）。结论停循环能使大鼠脑组织中HIF-1α和Smad2表达水平升高,深低温能促进停循环脑组织中HIF-1α和Smad2表达增加,发挥脑保护作用。Objective To study the expressions of hypoxia-inducible factor-1alpha（HIF-1α）and signal transduction molecule2（Smad2）in the brain of rats with deep hypothermic circulatory arrest,and to explore the roles of HIF-1αand Smad2 in deep hypothermia brain protection. Methods Thirty-nine SD rats were divided into deep hypothermic circulatory arrest group,room-temperature circulatory arrest group and room-temperature cyclic group,with 13 rats in each group.The rats in deep hypothermic circulatory arrest group received cardiopulmonary bypass（CPB）for 10 min followed by circulatory arrest for 10 min at rectal temperature below 20 ℃.The rats in room-temperature circulatory arrest group received CPB for 10 min at the rectal temperature 36.5to 37 ℃,followed by circulatory arrest for 10 min.The rats in room-temperature cyclic group received CPB for 20 min at rectal temperature 36.5to 37℃ without circulatory arrest.The histopathological changes of brain tissue were observed in 3groups.The expressions of HIF-1αand Smad2 protein in rat brain were detected by immunohistochemistry method.Results The HE staining results showed small swelled neurons of brain tissue,degenerated neuronal,proliferated glial cells,and infiltrated inflammatory cells inroom-temperature circulatory arrest group.The number and morphology of brain cells were normal and there were no obvious pathology changes in deep hypothermic circulatory arrest group and room-temperature cyclic group.The brain tissue HIF-1αand Smad2 were highly expressed in deep hypothermic circulatory arrest group,were moderately expressed in room-temperature circulatory arrest group,and lowly expressed in room-temperature cyclic group.The average gray values of HIF-1α（101.32±9.23）and Smad2（104.36±7.12）in deep hypothermic circulatory arrest group were significantly lower than those in room-temperature circulatory arrest group（123.35±7.26,113.42±7.33）and in room-temperature cyclic group（148.14±5.47,124.75±6.36）（P〈0.05）,and in room-temperative

关 键 词：深低温停循环 缺氧诱导因子-1Α 信号转导分子2 大鼠 

分 类 号：R651.15[医药卫生—外科学]