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目的探讨环孢素A对脑缺血再灌注损伤的保护作用。方法将108只大鼠分为假手术组、生理盐水对照组和环孢素A治疗组,参照Zealonga线栓法制备局灶性脑缺血再灌注模型,大鼠脑缺血2h再灌注22和70h后,分别对各组各时间点大鼠的行为学评分、脑TTC染色、缺血区IL-1β含量和MPO活性进行测定和观察,并对结果进行统计处理。结果各时间点环孢素A治疗组与对照组相比,环孢素A组行为学评分优于对照组(P<0.05);环孢素A组脑梗死灶体积比对照组明显减轻(P<0.05);环孢素A可有效降低大鼠局灶性脑缺血再灌后脑组织中IL-1β的含量(P<0.01);并可显著抑制MPO的活性(P<0.01)。与上述两组相比,假手术组各项观察指标则无明显异常改变。结论炎症反应参与脑缺血再灌注损伤,环孢素A可显著降低缺血再灌注后脑组织中IL-1β的含量、减轻缺血区内白细胞的浸润、对大鼠脑缺血再灌注损伤具有明显的保护作用。
Objective To investigate the protective effect of cyclosporin A on cerebral ischemia-reperfusion injury. Methods 108 rats were divided into sham-operation group, saline control group and cyclosporine A treatment group. According to Zealonga method, focal cerebral ischemia / reperfusion model was established. After 70h, the behavior scores, the brain TTC staining, the content of IL-1β in the ischemic area and the activity of MPO were measured and observed in each group at each time point, and the results were statistically analyzed. Results Compared with the control group, the cyclosporine A group had better behavioral scores than the control group (P <0.05). The volume of cerebral infarction in cyclosporine A group was significantly reduced (P <0.05). Cyclosporine A can effectively reduce the content of IL-1β in brain tissue after focal cerebral ischemia-reperfusion in rats (P <0.01), and inhibit the activity of MPO significantly (P <0.01). Compared with the above two groups, the sham operation group had no obvious abnormal changes in all the indicators. CONCLUSION: Inflammatory reaction is involved in cerebral ischemia-reperfusion injury. Cyclosporine A can significantly reduce the content of IL-1β in the brain tissue after ischemia-reperfusion, reduce the infiltration of leukocytes in the ischemic area and have the effects on cerebral ischemia-reperfusion injury in rats Obvious protection.