摘要
目的 研究地塞米松预处理对新生大鼠缺氧缺血性脑损伤时脑组织细胞间黏附分子 1(ICAM 1)的表达与白细胞浸润的影响。方法 将 4 8只新生大鼠制作成缺氧缺血性脑病 (HIE)模型 ,于制作模型前 2 4小时即分别予地塞米松预处理组和对照组大鼠腹腔内注射地塞米松 0 1mg/kg、生理盐水 10ml/kg。模型后2 4小时处死大鼠 ,分别进行脑组织ICAM 1免疫组织化学检测、白细胞计数及组织HE染色。结果 ICAM 1平均吸光度 :预处理组 (3 6 2± 1 2 1) ,对照组 (9 4 2± 2 6 5 ) (P <0 0 5 ) ;神经细胞损伤评分 :预处理组 (0 38±0 13) ,对照组 (1 6 3± 0 74 ) (P <0 0 0 1) ;白细胞浸润 :预处理组 (8 4± 1 7) ,对照组 (16 3± 4 6 ) (P <0 0 0 1)。结论 地塞米松预处理能减少HIE时脑组织的ICAM 1蛋白表达及白细胞浸润 。
Objective To investigate the influnce of dexamethasone pretreatment on the expression of ICAM 1 and neutrophil infiltration in brain tissue of hypoxic ischemic neonatal rats Methods Forty eight neonatal rats were made to model with hypoxic ischemic encephalopathy(HIE) The control group and the dexamethasone group were respectively injected intraperitoneally with normal saline 10 ml/kg, dexamethasone 0 1 mg/kg before hypoxia ischemia;all animals were killed 24 hours after hypoxia ischemia Immunocytochemistry was used to determine the absorbency of ICAM 1 The damage grade of neurocytes and leukocyte infiltration were recorded for the histopathological study Results Compared to the control group,the mean absorbency(A) of ICAM 1, the damage grade of neurocytes and neutrophil infiltration of the dexamethasone group were all obviously decreased( P < 0 05, P < 0 001, P < 0 001) Conclusion Dexamethasone pretreatment may decrese the expression of ICAM 1,leukocyte infiltration and cerebral damage regions of HIE
出处
《临床神经病学杂志》
CAS
2003年第5期287-288,共2页
Journal of Clinical Neurology
