急性进展性脑梗死患者外周血可溶性CD40配体及PBMC胞核NF-κB的表达  

Expression of sCD40L in peripheral blood and NF-κBp65 in PBMC of patients with acute progressive cerebral infarction

作　　者：毛德军[1] 郭瑞友[1] 唐咏春[1] 臧运华[1] 

机构地区：[1]青岛大学医学院附属海慈医疗集团神经内科,山东青岛266033

出　　处：《细胞与分子免疫学杂志》2011年第2期177-179,共3页Chinese Journal of Cellular and Molecular Immunology

基　　金：青岛市2007年医药科研指导计划项目资助(2007WSZD071)

摘　　要：目的:研究急性进展性脑梗死(APCI)患者外周血清可溶性CD40配体(sCD40L)水平及外周血单个核细胞(PB-MC)胞核核因子κB(NF-κB)p65表达率的变化。方法:采用前瞻性研究方法选择起病7d以内的99例APCI患者作为APCI组,选择同期急性脑梗死(ACI)患者及门诊查体的脑动脉硬化(CAS)患者各100例分别作为ACI组和CAS组;CAS组于查体时,APCI组及ACI组于入院时、病程第7天、第14天、第30天分别监测患者外周血清sCD40L及PBMC胞核NF-κBp65表达率的变化。结果:ACI组入院时外周血清sCD40L及PBMC胞核NF-κBp65表达率均明显高于CAS组(P<0.05),APCI组于入院时、病程第7天、第14天及第30天外周血清sCD40L及PBMC胞核NF-κBp65表达率均明显高于ACI组(P<0.05)。结论:CD40-CD40L信号通路及PB-MC胞核NF-κB表达的过度上调而介导的炎症、凋亡机制可能是APCI发生与发展的分子生物学机制之一。AIM： To study the expressional changes of soluble CD40 ligand （sCD40L） in peripheral blood serum and nuclear factor-kB （NF-kB） p65 in peripheral blood mononuclear cells （PBMC） of patients with acute progressive cerebral infarction （ APCI ）. METHODS： We selected ninety-nine patients getting APCI less than 7 d of the onset as APCI group by prospective method. Each 100 cases of patients with acute cerebral infarction （ACI） in the same and with cerebral arteriosclerosis （CAS） in the outpatient were respectively selected as ACI and CAS group. The expressional changes of sCD40L in peripheral blood serum and NF-KBp65 in PBMC of patients with CAS on admission, of patients with APCI and ACI when in hospital, on the course of seventh day, of fourteen and of thirtieth were detected respectively. RESULTS.. The expression of sCD40L in peripheral blood serum and NF-KBp65 in PBMC of patients of ACI group on admission were obviously higher all than that of CAS group （ P 〈 0.05） ; The expression of sCD40L in peripheral blood serum and NF-KBp65 in PBMC of patients of APCI group when in hospital, on the course of seventh day, of fourteen and of thirtieth were obviously higher all than that of ACI group （ P 〈 0.05 ）. CONCLUSION： The inflammatory and apoptotic mechanism mediated by expressional excessive increase of CD40-CD40L signal passage and NF-KB in PBMC might be one of the molecular biology mechanisms of onset and Droaress for APCI.

关 键 词：脑梗死 CD40配体 核因子ΚB 

分 类 号：R743.32[医药卫生—神经病学与精神病学]