| Objective:To explore the changes of tumor necrosis factor-alpha (TNF-α) ,interleukin-1β (IL-1β) ,interleukin-6 (IL-6),interleukin-8 (IL-8) ,malondialdehyde (MDA) and superoxide dismutase (SOD) and the effects of propofol on these cytokines in rats following cerebral ischemia- reperfusion injury. Methods:Focal cerebral ischemia model was induced with occluding the middle cerebral artery (MCA). Seventy two adult Wistar rats were divided randomly into three groups: sham operation group (group A), control group ( group B)were divided into four groups, all brain ischemia for two hours and reperfusion for one hour, six hours, twelve hours ,twenty-four hours after ischemia respectively, which were intrapentoneally infused 0.9% saline (10ml/kg) before ischemia and reperfusion. Propofol group (group C ) was intrapentoneally infused propofol (100mg/kg) before ischemia and reperfusion. The serum concentration of TNF-α,IL-1β,IL-6,IL-8 and malondialdehyde(MDA) contents and activities of superoxide dismutase (SOD) of the brain tissue were measured. Hematoxylin and eosin staining for the cerebral tissue was processed.Results:TNF-α,IL-1β,IL-6,IL-8 in plasma of group B and group C after ischemia-reperfusion were higher than group A(P<0.05) ,But the levels of group C were significantly lower than that of group B (P<0.05). MDA levels of group C were significantly lower than that of group B. But the changes of SOD were contrary to those of MDA in group B and C .Under light microscope and electron microscope ,the structure of nerve cell of cerebral cortex of group C was better than group B, and the nerve cell of group B was swelling,karyorrhexis,karyolysis. Infarction area of brain was significantly smaller in group C than group B.Conclusion:These inflammatory cytokines play an important role in secondary injury of cerebral ischemia and reperfusion. Inaddition to antioxidantion, propofol suppresses effectively the production and release of these inflammatory cytokines and MDA, facilitates the production of SOD, and decreases the infarction area of brain, to protect the brain from ischemia and reperfusion injury. ... |