大鼠局灶性脑缺血再灌注损伤的炎症机制及药物干预

The Inflammtory Mechanism of Focal Cerebral Ischemia reperfusion Injury in Rats and Drug Therapy

目的 研究大鼠局灶性脑缺血再灌注损伤的炎症反应机制 ,以及免疫抑制剂甲基强的松龙和非选择性腺苷受体激动剂 2 CAdo对炎症反应的影响。方法 采用线栓法制备大鼠局灶性脑缺血再灌注模型。检测缺血1h再灌注 2 3h后皮质肿瘤坏死因子 α(TNF α)、丙二醛 (MDA)、微血管内中性粒细胞计数及血清胞浆酶CK、CK BB、LDH含量的变化。结果 大鼠局灶性脑缺血再灌注后皮质TNF α及MDA含量增加 ,胞浆酶水平增高 ,微血管内白细胞聚集、浸润。甲基强的松龙及 2 CAdo可降低皮质TNF α的表达 ,使MDA含量下降 ,胞浆酶水平降低 ,并减轻微血管内白细胞的聚集、浸润。结论 急性炎症反应与局灶性脑缺血再灌注组织损伤有关。甲基强的松龙与 2 CAdo具有抑制局灶性脑缺血再灌注时的炎症反应 ,减少过氧化物的产生 ,稳定神经细胞膜的作用。

Objective To study the inflammtory mechanism of focal cerebral ischemia reperfusion injury in rats,and the effect of immunoinhibitor methylprednisolone or nonselective adenosine receptor against 2 chloroadenosine on them.Methods The focal cerebral ischemia reperfusion model was established with thread embolism of middle cerebral artery. The levels of TNF α and MDA in cortex, the changes of serum cytosolic enzymes,leukocyte accumulation and adhesion were observed after 1 h ischemia and 23 h reperfusion.Results After focal cerebral ischemia reperfusion, the levels of TNF α,MDA and serum cytosolic enzymes were significantly increased, leukocyte accumulation and adhesion was improved. Infusion of methylprednisolone or 2 chloroadenosine can make all decreased.Conclusions Acute inflammtory mechanism was related with focal cerebral ischemia reperfusion injury. Methylprednisolone or 2 chloroadenosine can inhibit inflammtory reaction and superoxide production, make nerve cells membranae stable.