Abstract： Objective To investigate the impact of the ischemic postconditioning on the tumor necrosis factor (TNF)-α/IL-6/signal transducers and activators of transcription (STAT)-3 signal pathway of liver regeneration.Methods Ninety healthy clean grade male Spragne-Dawley rats weighting 230 to 280 g were selected and assigned into three groups randomly:group Ⅰ subtotal hepatectomy ( SH ),group Ⅱ ischemia reperfusion (IR),group Ⅲ ischemic postconditioning (IPO).The left and middle liver was resected,and the remnant liver was treated as followed:the blood flow was not blocked in SH group,but blocked 30 minutes in IR group,then reperfused ; IPO groups received three cycles of 30 s-30 s intermittent interruptions of blood flow at onset of reperfusion. At 1,6,12,24,48 h after reperfusion,the serum TNF-α,IL-6 was detected and the mRNA of cyclinD1,Cdk4,STAT-3 was assayed by real-time PCR as well as the protein expression of cyclinD1 and Cdk4 by Western blot.Results Compared with SH group,the expression of IL-6 declined at each set time point in IR group ( t =5.076 to 8.334,P =0.000),but the content of TNF-α increased in early stage ( 1 to 12 h) ( t =2.972 to 7.215,P =0.000-0.014).The expression of STAT-3,cyclinD1 and Cdk4 mRNA and protein of cyclinD1 and Cdk4 at 24 and 48 h after reperfusion were lower in IR group than in SH group ( t =2.857 to 6.684,P =0.000 to 0.017 ).However,there was a significant decrease in TNF-α from 1 to 12 h after reperfusion ( t =2.995 to 4.112,P =0.002 to 0.017),but a significant increase in IL-6 in IPO group than in IR group (t =2.458 to 3.543,P =0.005 to 0.034).The expression of STAT-3,cyclinD1,Cdk4 mRNA and protein of cyclinD1 and Cdk4 at 24 and 48 h after reperfusion were all increased in IPO group in comparison with in IR group ( t =2.383 to 6.803,P =0.000 to 0.038 ).Conclusions The ischemic postconditioning could promote the remnant liver regeneration after subtotal hepatectomy with ischemia reperfusion injury.Its mechanism relates with the activation of the TNF-α/IL-6/STAT-3 signal pathway of and the cyclinD1-Cdk4 complex which enhances the proliferation of hepatocyte.