Effects of r - HuEPO on expression of NF - κB and IκB in focal cerebral ischemia/reperfusion in rats

Objective To explore the function of NF - κB and IκB in the neuroprotection of EPO on inflammatory injury induced by cerebral focal ischemia/reperfusion in rats.Method Thread embolism was performed to establish cerebral ischmia/reperfusion model in rats.Immunohistochemistry and Western blot were employed to determine the expression of NF - κB and IκB in the ischemic context,respectively.The amount of IL - 1β protein was detected by ELISA.Results Compared with sham,the amount of IL - 1β protein was significantly induced in ischemic tissue.The expression of IL - 1β was increased to ( 86.2 ± 25.2) pg/ml and ( 867.2 ± 74.3 ) pg/ml at 3 h and 24 h of I/R ( P ＜ 0.01 ).The high level of IL - 1β expression was continued after 72 h I/R we observed.The administration of EPO significantly reversed the IL -1β expression induced by I/R at 3 h,6 h,12 h and 24 h.Compared with IL- 1β levels at different time points in I/R group,the amount of IL - 1β protein in EPO group decreased by 55％,33％,56％,50％ ( P ＜0.01 ).The expression and activation of NF - κB p65 was 4 - 13 folds higher in I/R groups in comparison with sham group at every time points.Interestingly,the expression of NF - κB p65 was remarkably decreased about 33％ ～40％ ( P ＜0.01 ) in EPO group compared with L/R group.Interestingly,Western blot showed that the amount of IκBαt inhibited by I/R was induced by the administration of EPO after I/R.The level of IKB increased by 11％,34％,83％,40％,23％,20％ at every time point.Conclusions EPO may be a protective molecule by inhibiting NF- κB/IκB signalling pathway,decreasing the synthasis and secretion of IL- 1β. Key words: Erythropoietin, recombinant;  Brain ischemia;  Reperfusion;  NF - kappa B; Inhibitory κB