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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。结论：抗ＴＮＦ－αｍＡｂ能减轻短暂性脑缺血损害
During the process of cerebral ischemia, a large amount of TNF-α was expressed, and TNF-α involved in and promoted the process of brain damage. The purpose of this study is to use anti-TNF-α mAb inhibit the expression of TNF-α and its biological activity, so as to protect the brain tissue, MCA occlusion model in rats. Twenty-six rats were randomly divided into two groups. One group was given anti-TNF-α mAb and the other group was given the same amount of saline as control. The infarct volume, leukocyte attachment, aggregation and tissue infiltration were observed. As a result, it was found that anti-TNF-α mAb significantly reduced infarct volume in transient ischemic attack and microscopic examination revealed that it significantly reduced leukocyte aggregation and adhesion during reperfusion, thereby protecting brain tissue. Conclusion: Anti-TNF-α mAb can reduce transient ischemic damage