Object To investigate the inhibitory effect of interleukin-10 on the expression of ICAM-1,P,E-selectin and nuclear factor kappa B and its molecular mechanisms in focal cerebral ischemia-reperfusion in rats.Methods Adult male Sprague-Dawley rats were randomly assigned into 4 groups,Sham group,Ischemia-Reperfusion group,Vehicle group and IL-10 group.Rats'Ischemia-Reperfusion model was induced by Zea- Longa's thread method, and IL-10 was administered intracerebroventricularly 1h post MCAO. Immunohistochemical staining and RT-PCR were used to detect the expression of ICAM-1,P,E-selectin ,and immunohistochemical staining were used to detect the expression of NF-κB in peri-infarct.Results ICAM-1,P,E-selectin and NF-κB predominantly expressed in the striatum and sub-frontal/parietal cortex at the border of the infarct core following cerebral ischemia-reperfusion in rats. ICAM-1,P,E-selectin expressed on capillary vessel endothelial cell .NF-κB expressed in cytoplasm in sham operated group,and it was partly expressed in the nucleus after cerebral ischemia-reperfusion. Compared with sham group,the expression of ICAM-1,P,E-selectin and NF-κB were significantly upregulated in cerebral ischemia-reperfusion group ( p<0.01);Compare with vehicle group, the expression of ICAM-1,P,E-selectin and NF-κB were significantly downregulated in IL-10 group (p<0.05 or p<0.01).Conclusions:1 Cerebral ischemia-reperfusion in rats significantly upregulated the expression of ICAM-1,P,E-selectin and NF-κB,which indicated that ICAM-1,P,E-selectin and NF-κB involved in the inflammatory reactions following cerebral ischemia -reperfusion,leading to the inflammatory reactions following cerebral ischemia-reperfusion damage.2 IL-10 could downregulate the expression of ICAM-1,P,E-selectin and NF-κB, which sugguested that IL-10 could inhibit inflammatory reaction following cerebral ischemic-reperfusion .
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