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凝闭大鼠一侧大脑中动脉，造成局灶性脑梗塞后２４小时，大鼠外周中性粒细胞活性增强；缺血区脑组织脂质过氧化损伤严重；ＴＴＣ染色后可见边界明显的脑坏死区。地塞未松可抑制脑缺血所致的中性粒细胞吞噬化学发光增强，减少白细胞在缺血区的浸润，减轻组织脂质过氧化损伤，保护ＳＯＤ活性，缩小梗塞范围。其抑制粒细胞功能激活与减轻脑缺血性损伤之间有显著的正相关关系。提示：脑梗塞时，激活的外周白细胞能加重脑缺血性损伤；地塞米松抑制白细胞功能的作用可能是其防治脑梗塞的机制之一。
The middle cerebral artery was closed in one side of the rat, causing the peripheral neutrophil activity to increase 24 hours after focal cerebral infarction. The lipid peroxidation in the ischemic area was severely damaged. After TTC staining, the brain with obvious border Necrosis area. Dexamethasone can inhibit cerebral ischemia induced neutrophil phagocytosis chemiluminescence increased, reduce the infiltration of leukocytes in the ischemic area, reduce tissue lipid peroxidation damage, protect SOD activity, reduce infarct size. There was a significant positive correlation between the inhibition of granulocyte activation and alleviation of cerebral ischemic injury. Tip: When infarction, activation of peripheral white blood cells can aggravate cerebral ischemic injury; dexamethasone inhibition of leukocyte function may be one of the mechanisms of prevention and treatment of cerebral infarction.