Abstract:Objective:To investigate the influence of oleanolic acid(OA) pretreatment to rat’s IKK/I-κB/NF-κB signaling pathway around its hepatic ischemic/reperfusion injury(HIRI). Methods:One hundred and twenty eight male Sprague-Dawley (SD) rats were randomly divided into sham group(SH),ischemic/reperfusion group(IR),0.5% sodium carboxymethycellulose(CMC-Na) group(CM) and OA+0.5% CMC-Na group(OA). Before the operation,the rats of each group received intragastric administration of corresponding solution once a day for seven days(OA group with 100 mg/kg of OA dissolved in 0.5% CMC-Na,SH group and IR group with water of the same volume,CM group with 0.5% CMC-Na of the same volume). At the 8th day,rats were suffered from segmental(70%) hepatic ischemia for 60 min and then followed with different periods of reperfusion. The hepatic tissue were obtained at 0 h,3 h,and 6 h after the reperfusion. The expression of IKK2 and I-κBα in the cytoplasm and NF-κB p65 in the nucleus were evaluated by the method of Western blotting. Results:There was no IKK2 expression in the cytoplasm,and only few of NF-κB p65 was detected in the nucleus before operation or 0h after reperfusion in each group. Meanwhile,the volume of I-κBα detected in the cytoplasm has no significant difference among four groups at the same point of time. The expression of IKK2 in the cytoplasm and NF-κB p65 in the nucleus in the SH group was much lower than those in other three groups(P < 0.05),while those proteins detected in OA group is less than those in CM group and IR group(P < 0.05)at 3h or 6 h after reperfusion. At these two points of time,the expression of I-κBα in SH group was higher than that in the other three groups(P < 0.05),and this protein detected in OA group is more than that in CM group and IR group(P < 0.05).The expressions of IKK2 and I-κBα in the cytoplasm and NF-κB p65 in nucleus between CM group and IR group had no significant difference at each point of time(P > 0.05). Conclusion:HIRI would increase the expression of IKK2 in the cytoplasm,leading to the phosphorylation of I-κB,activating NF-κB and making it to translocate into the nucleus,and then the activated NF-κB which could mediate inflammatory response eventually caused damage of liver cells. The pretreatment of OA can inhibit the activating of the signaling pathway of IKK/I-κB/NF-κB,which may be one of the mechanisms for OA alleviating HIRI.