Ischenic postconditioning down-regulates expressions of interleuldn-1β and tmnor necrosis factor-a in cerebral ischemia/reperfusion in rats

Objective To investigate the effects of ischemic postconditioning （IP） on interleukin-1β （IL-1β） and tumor necrosis faetor-ct （TNF-α） expression in focal cerebral ischemia/reperfusion in rats in order to clarify the mechanism of neuroprotective effect of IP. Methods One hundred and ten healthy adult male Sprague-Dawley rats were randomized into sham operation （n = 10）, ischemiaJreperfusion and IP groups. The latter two groups were redivided into 6-, 12-, 24-, 48- and 72-hour subgroups （n = 10 in each subgroup） according to their reperfusion time. A focal cerebral ischemia/reperfusion model was induced by the middle cerebral artery intraluminal suture method. After middle cerebral artery occlusion for 2 hours, reperfusion for 15 seconds was conducted using the IP method, and this was repeated for 3 times. The neurobehavioral scores of the rats were evaluated in each group. The infarct volume was measured with 2,3,5-triphenyltetrazolium chloride staining. The expression of TNF-oL and IL-1β protein in brain tissue was detected by immunohistochemistry assay. The expression of IL-1β and TNF-ctmRNA was determined by in situ hybridization. Results Compared with the ischemia/reperfusion group, the neurobehavioral score and and cerebral infarct volume in the IP group decreased significantly （all P 〈0. 05）. Expressions of IL-1β,TNF-α protein and mRNA were slight in the front- oparietal cortex in the sham group; however, they were apparent in ischemia/reperfusion group and 1P groups,and began to increase at 6 hours and reached the peak at 24 hours （compared to other time points all P 〈0. 05）, then decreased gradually. There was the same dynamic change trend in the IP ffoup, and the expression at each time point was siguificantly lower than that in the ischemia/reperfusion group （all P 〈 0. 05）. Conclusions IP significantly down-regulates the expressions of IL-1β and TNF-α and reduces the infarct volume of the ischemia/reperfusion in rats. These findings indicate that IP may play a neuroprotective role by inhibiting the inflammatory reslaonse in brain tissue after ischerniaJreoerfusion. Key words: Brain Ischemia;  Ischemic;  Preconditioning Reperfusion Injury;  Interleukin-1β;  Tunor Necrosis Factor-α;  Disease Models, Anirml;  Rats