| The cerebrovascular disease is the common disease intimidateshuman's health, With characters of high attack rate, high death rate,high mutilation, high relapse rate and many complication. Prevalencerate of the cerebrovascular disease is 200/100 thousand per year, morethan 2 million persons fall ill per year in our country. More than 45%persons succumb to the cerebrovascular disease, Now, our country payfor it almost RMB 200,000 million, it brings heavy burden togovernment and family. So it becomes an important topic of of thecerebrovascular disease. The mechanism and the prevention and cure of secondarydamage to nerve injury after acute ischemic of the cerebra is the hotspot cared. To research efficacious nerve protector, master accuratetime, and prevent ischemic semidarkness to continue injury is theresearching hot spot, may be the breakthrough of the treatment toischemic cerebral stroke. The mechanism of cerebral ischemic damage is very complicated.Many factors take part in the injury of neuron. In them, interleukin isclearly. Interleukin-8,IL-8 is a tendency interleukin that can activateneutrophilic granulocyte, induce neutrophilic granulocyte to deform,tendency, degranulation, Ca2+ inter cell grow up transient, synthesislipoid with biological activity, integrin grow up, respiratory outbreak.This experiment intend to confirm the importance of IL-8 act astendency factor in the damage of cerebral ischemic reperfusion, to findthe time to interfere in earlier, and to reduce the damage of cerebralischemia.We adopted the thread-embolism in male Wistar rats to producethe acute ischemia. We observed the changes of IL-8 both in the brainand the blood serum in the different time after the operation withELISA method, research the pathological appearance and the action ofcytokines in it. We approach the mechanism of the acute damage byinflammation in cerebral ischemia.Here are the results:1. We used 0.225 mm nylon fish thread as embolus, and finishedin 30 minutes to Wistar rat. TTC staining confirm thatachievement ratio high. The human being is commonly inMCAO, so as the rats we deal with. So we can consider therats embolismed with thread is the better one.2. IL-8 in the brain is growing up after 1 hour of ischemia, andreaching the peak after 24 hours, then going down. But it islower than control and blank rats. IL-8 in the blood serum isgrowing up after 1 hour of ischemia, and reaching peak after 4hours, and going down steady.3. While the group of intervention with the Dexamethasone,IL-8 in the brain and in the blood serum is lower than withoutthe Dexamethasone.In a brief, we occluded the content of IL-8 in the brain is growingup after 1 hour of ischemia, and reaching the peak after 24 hours, thengoing down. But it is lower than control and blank rats.So the 24thhour may be the right time to deal with the inflammation. And IL-8may play two parts in the reaction. One is to mediate physiologicalreaction, the other is to make neutrophilic granulocytes mediatinginjury in ischemia. The result of the group with the Dexamethasoneproof that glucocorticosteroid can reduce quantity of T lymphocytes,histoleucocytes, eosinophilic granulocytes;depress proliferation oflymphocytes and generation of cytokines;depress differentiation andactivity of macrophages;depress sticky of neutrophilic granulocytes;degrade permeation of vascular, thereby deduce injury ofinflammation .From the total experiment we can conclude:(1) the thread-embolism is a reliable method to to produce theacute ischemia.(2) IL-8 in both the brain and the blood serum, is correlated withtime in acute cerebral ischemia.(3) The Dexamethasone can depress inflammatory reaction of thebrain in acute cerebral ischemia obviously.
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