摘要
目的:探讨抗巨噬细胞活化趋化因子1(Mac1)抗体保护神经元缺血性损伤的作用机制。方法:24只Wistar大鼠随机分为4组:正常对照组(4只)、伪手术组(4只)、脑缺血再灌注损伤组(脑缺血组,8只)、脑缺血再灌注损伤加Mac1抗体实验组(脑缺血加抗体组,8只)。分离培养鼠脑毛细血管内皮细胞(CCEC)和多形核白细胞(PMN),利用微管吸吮技术,观察PMN与CCEC间粘附力学特性的变化。结果:脑缺血再灌注后各时间点,PMN与CCEC粘附力和粘附应力均明显高于正常对照组和伪手术组(P均<0.01);加抗Mac1抗体后,细胞粘附力和粘附应力均明显下降(P<0.05或P<0.01)。结论:脑缺血再灌注损伤后抗Mac1抗体使PMN与CCEC粘附力减小,粘附应力下降;
Objective:To investigate the potential mechanism underlying the protective effect of antimacrophage activating chemokine(Mac)1 antibody on ischemic neuron damage.Methods:Twentyfour Wistar rats were randomly divided into 4 groups:normal controls (n=4),sham operation group (n=4),cerebral ischemia group (n=8),and treatment group (antiMac1 antibody,n=8).Polymorphonuclear leukocytes (PMN) were separated from the blood ,and antiMac1 antibody was used to assay its inhibitory effect on adhesion between PMN and cultured cerebral capillary endothelial cells(CCEC) in vitro using micropipette aspiration technique after cerebral ischemiareperfusion.The mechanical properties of adhesion between PMN and CCEC cells were investigated in this study.Results:Following cerebral ischemiareperfusion,adhesion force and adhesion stress between PMN and CCEC were significantly elevated compared to normal controls and sham operation group (both P<001).Treatment with antiMac1 antibody,however,both adhesion force and adhesion stress were markedly reduced (P<005 or P<001).Conclusions:AntiMac1 antibody could reduce adhesion force and adhesion stress between PMN and CCEC after cerebral ischemiareperfusion damage.In view of its inhibitory effect on adhesion between PMN and CCEC cells,it is suggested that the application of antiMac1 antibody may be used in the treatment of ischemic cerebral vascular diseases.
出处
《中国危重病急救医学》
CSCD
1998年第4期204-206,共3页
Chinese Critical Care Medicine
基金
国家自然科学基金
关键词
再灌注损伤
内皮细胞
脑缺血
MAC-1
cerebral ischemiareperfusion injury\ \ polymorphonuclear leukocyte endothebial cell
antimacrophage activating chemokine1 antibody