摘要
脑缺血过程有大量TNF-α的表达,TNF-α参与和促进了脑损害的过程。本研究的目的为用抗TNF-αmAb抑制TNF-α的表达及其生物活性,从而达到保护脑组织的作用,采用大白鼠MCA堵塞模型。将缺血6小时大白鼠16只随机地分为两组,一组给予抗TNF-αmAb,另一组给予等量生理盐水作对照;观察梗塞体积大小,白细胞附壁、聚集及组织浸润情况。结果发现抗TNF-αmAb显著减少短暂性脑缺血的梗塞体积,显微镜观察发现能显著减少再灌注时白细胞聚集和粘附,从而保护脑组织。
There are a great amount of TNF-α expression after cerebral ischemia.TNF-α plays a critical role in leukocyte infiltration and tissue injury. The purpose of the present study was to inhibit expression and activities of TNF-α using Anti-TNF-αmAb for protection brain tissue. Rat MCAO model was applied ,in which the rats were subjected to six hours of ischemia and treated respectively with Anti-TNF-αmAb and NS after reperfusion and were killed 24hours after onset of ischemia.Result showed that AntiTNFαmAb reduced significantly the volume of the ischemic lesion and inhibited leukocytes adhesion and reduced leukocytes accumulation in microcirculation. The authors concluded that Anti-TNF-αmAb could protect transient cerebral ischemia.
出处
《卒中与神经疾病》
1998年第2期81-84,共4页
Stroke and Nervous Diseases
关键词
再灌注
脑缺血
TNF-Α
单克隆抗体
Focal cerebral ischemia Tumor necrosis factor-α Monoclonal antibody Leukocytes adhesion、accumulation