EFFECTS OF ISCHEMIC POSTCONDITIONING ON TNF-α AND IL-1β EXPRESSION IN RATS AFTER CEREBRAL ISCHEMIA/REPERFUSION

Objective To investigate the effects of ischemic postconditioning on expression of tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in rat models of focal cerebral ischemia/reperfusion.Methods This study consisted of 110 adult healthy male Sprague-Dawley rats.They were randomized to sham-operation group(n=10),the rest 100 were evenly divided into ischemia-reperfusion group(I/R group) and ischemia-postconditioning group(IP group).The latter two groups were subdivided into five subgroups according to different time points of I/R as 6-,12-,24-,48-and 72-hour groups,with 10 of each group.A model of focal cerebral ischemia-reperfusion was created by intraluminal threading of middle cerebral artery occlusion(MCAO) and IP for 2 h,then reperfusion for 15 seconds,followed by ischemia for 15 seconds,which was repeated for three times.Each group was evaluated for neuroethology,TTC staining of the volume of the infarcion,immunohistochemical method was employed for the expressions of TNF-α and IL-1β protein,and in situ hybridization for TNF-α and IL-1β mRNA expressions.Results The neurobehavioral deficit and cerebral infarction were seen in the I/R and IP group,as compred between them,the vo-lume of infarction was smaller,and the neuroethology improved in IP group(t=2.683-5.657,P0.05).Slight expressions of TNF-α and IL-1β could be found in the frontoparietal lobe in the sham-operation group,but the expressions in I/R and IP group started to rise at six hours of reperfusion,reaching their peak at 24 hours.Compared with corresponding subgroups of I/R,the expressions of TNF-α,IL-1β protein and mRNA in IP group declined significantly(t=2.333-7.814,P0.05).Conclusion IP down-regulated the expressions of TNF-α and IL-1β,reducing the volume of cerebral infarction,which indicates that IP can inhibit inflammation caused by ischemia-reperfusion and play a role in the neuroprotective effect.