| Objective We will observe the expression of FKN,MCP-1and TNF-α in focal cerebral ischemia and reperfusion penumbra,to investigate the time course changes regulation of the three factors in the inflammation of cerebral ischemia-reperfusion injury.Methods102healthy male Sprague-Dawley rats, weighting250～300g, were used in this study and divided randomly into nine groups: The normal group(n=6), the sham-operation group (n=12), I2h/R3h (n=12), I2h/R6h (n=12), I2h/R12h (n=12), I2h/R24h (n=12), I2h/R48h (n=12), I2h/R72h (n=12), I2h/R7d (n=12). The cerebral ischemia reperfusion model was established by intraluminal thread occlusion of the middle cerebral arteries occlusion(MCAO),And we assessed the changement of neuronal deficits of rats after surgery. Through observing the morphological changes of the Nissl bodies to evaluated the pathologic changes,and detected the expression of FKN,MCP-1, TNF-α in the ischemic brain tissue by immunohistochemistry.The changes of FKN protein expression level were detected by western-blot method.Results1. There were no obvious significance of structure between the normal group and the sham-operated group, the number of Nissl bodies of group I2h/R3h and I2h/R6h reduced gradually,contrast with the normal group and the sham-operated group, there were no significant differences (P>0.05).The number of Nissl bodies of group I2h/R12h, I2h/R24h, I2h/R48h, I2h/R72h and I2h/R7d reduced siginificantly (P<0.05)2. The results of immunohistochemistry examines showed that: The expressions of TNF-α in the normal group and the sham-operated group were low, and there were no significant differences among the two groups (P>0.05). The expressions of TNF-α increased from early stage(I2h/3h)(P<0.05), peaked at24h (P<0.05),and then decreased gradually, the expressions of TNF-α in group of I2h/7d regressed to the baseline (P<0.05). The chemokine FKN was expressed in a low level in the normal group and the sham-operated group,and there were no significant differences among the two groups (P>0.05).The expression of FKN in model group increased from after3h reperfusion (P<0.05),peaked at24h (P<0.05),and then decreased gradually,the expression of FKN in group T2h/R7d was no higher than the normal group (P>0.05). The chemokine MCP-1was expressed very few in the normal group and the sham-operated group,and there were no significant differences among the two groups (P>0.05).The expressions of MCP-1in model group increased from after6h reperfusion (P<0.05),peaked at48h (P<0.05),and then decreased gradually, the expression of MCP-1in group T2h/R7d was no higher than the normal group (P<0.05)3. The results of Western-blot showed that:FKN was expressed in a low level in the sham-operated group, the expression was up-regulated in group I2h/R3h (P<0.05),peaked at24h (P<0.05),was still in a high level in group I2h/R3h (P<0.05).In group T2h/R7d there was no higher than the sham-operated group (P>0.05)Conclusions1.There was a high expression level of TNF-α at the early stage of the inflammation process, indicated that TNF-α may start and promote the inflammation post ischenic/reperfusion.2. The expression of FKN and MCP-1were up-regulated after focal cerebral ischemia/reperfusion,and changed dynamically,indicated that the two such factors may participate in the inflammatory process after cerebral ischemia-reperfusion injury.3. The time of the expression of MCP-1elevating and reaching its peak was a little delayed,indicated that it had connection with Monocyte clearing the necrotic tissue,promoting nerve repair after cerebral ischemia-reperfusion injury. |
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