| Objective To investigate the role of apoptosis-induced protein Omi/HtrA2 in tubular cell apoptosis induced by renal ischemia-reperfusion injury (IRI) in rats.Methods Male Wistar rats were randomly divided into five groups: sham-operated group, I-R 1 group, I-R 2 group, I-R+Ucf-101 1 group, I-R+Ucf-101 2 group. Rats except the sham were subjected to 45 min of renal ischemia by clamping both renal arteries with non-traumatic vascular clamps. The animals were treated with vehicle or Ucf-101(1.5μmol/kg) by peritoneal injection 10 min before reperfusion (I-R 2 group or I-R+Ucf-101 2 group) or 1 h of reperfusion (I-R 1 group or I-R+Ucf-101 1 group), respectively. Rats were sacrificed at 24 h of reperfusion. Both kidneys were harvested for further analysis. Tubular cell apoptosis was detected by terminal deoxynucleotidyl transferase(TdT)-mediated dUTP-biotin nick end labeling(TUNEL)assay. The activity of renal caspase-3 was confirmed by colorimetric method. Western blot was used to detect protein expression of renal Omi/HtrA2 protein.Results 1. Renal IRI induced a significant increase of protein expression of renal mature Omi/HtrA2, accompanied by increased activity of renal caspase-3 and increased number of cell apoptosis. 2. Ucf-101, the specific antagon of Omi/HtrA2, peritoneal injection 10 min before reperfusion, could inhibited the increased number of cell apoptosis and the activity of caspase-3, while, had no effects on both them, peritoneal injection 1h of reperfusion. 3. Statistical correlations were established between mature Omi/HtrA2 and the percentage of cell apoptosis(r=0.718, P<0.001).Conclusions The apoptosis-induced agent Omi/HtrA2 plays an important role in cell apoptosis induced by renal IRI. Blocking the expression of Omi/HtrA2 10 min before reperfusion could decrease cell apoptosis in renal IRI.
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