急性实验性脑出血大鼠缺血皮质区炎性因子的表达  

Expression of Inflammatory Factors in Ischemic Cortex of Rat Brain after Experimental Acute Intracranial Hemorrhage

作　　者：曾锦旗[1] 彭泽峰[2] 

机构地区：[1]温州医学院附属第一医院神经内科,浙江温州325000 [2]中南大学湘雅医学院附属第一医院神经外科,湖南长沙410008

出　　处：《中国神经免疫学和神经病学杂志》2004年第2期94-97,共4页Chinese Journal of Neuroimmunology and Neurology

基　　金：国家自然科学基金资助项目 ( 3 93 70 2 61)

摘　　要：目的　研究急性脑出血大鼠血肿周围与对侧缺血皮质细胞凋亡以及 HSP70与 NF-κB表达。方法　将大鼠随机分为正常组与模型组。用 型胶原酶立体定位法复制出血性卒中动物模型 ,术后 1、3、7d分别进行 HE染色、TUNEL染色、HSP70与 NF-к B免疫组化反应。结果　脑出血后 1 d于血肿周围缺血半暗区可见大量坏死细胞 ,HSP70与 NF-к B表达增强 ,出血对侧皮质细胞以凋亡改变为主 ,均于 3 d达高峰 ,7d仍有升高。结论　急性脑出血大鼠的缺血性损害于双侧均可见到 ,以血肿侧严重 ,损伤于 3 d达高峰 ,7d持续存在 ,脑出血后的继发性损害持续存在。Objective To observe the apoptosis and expression of HSP70 and NF-κB in ischemia cortex of rat brain after experimental intracerebral hemorrhage. Methods Rats were randomly divided into normal group and model group . Haemorrhagic stroke rat model was made by injecting collagenase type Ⅶ stereotaxically, observation was scheduled into three time point at 1 day, 3 days and 7 days after operation,on light microscope study with TUNEL HSP70, and NF-кB immunohistochemistry. Results A large number of dead cell were seen in ipsilateral ischemic cortex, expression of HSP70 and NF-кB were both enhanced, apoptosis were mainly seen in contralateral ischemia cortex, all changes peaked at 3 day, and kept higher until 7 days. Conclusions Ischemia damage occurs in both sides after acute cerebral hemorrhage which is more severe in hematoma side, damage gets to peak in 3 days, keeps high in 7 days,and ischemia damage persists after intracerebral hemorrhage.

关 键 词：急性实验性脑出血 大鼠 缺血皮质区 炎性因子 免疫组化 

分 类 号：R743.34[医药卫生—神经病学与精神病学]