Objective To evaluate the effect of ulinastatin on neuronal apoptosis in spinal cord af-ter peripheral nerve injury in mice. Methods A total of 225 healthy male SPF C57BL∕6J mice, aged 6-8 weeks, weighing 18-22 g, were divided into 3 groups ( n=75 each) using a random number table method:sham operation group ( group Sham), peripheral nerve injury group ( group PNI) and ulinastatin group ( group UTI) . The model of unilateral sciatic nerve transection was established in PNI and UTI groups. Uli-nastatin 10000 U∕kg was injected intraperitoneally once a day for 3 consecutive days in group UTI, while the equal volume of normal saline was given instead in Sham and PNI groups. The mice were sacrificed at 1, 3, 7, 14 and 28 days after administration ( T0-4 ) , and the L4-6 segments of the spinal cord were re-moved for examination of the pathological changes ( under the light microscope ) and for determination of neuronal apoptosis (by TUNEL) and expression of caspase-12, Bcl-2, Bax and activated caspase-3 (by Western blot) and expression of caspase-12 mRNA ( by real-time polymerase chain reaction) . Apoptosis in-dex ( AI) and Bcl-2∕Bax ratio were calculated. Results Compared with group Sham, AI was significantly increased, the expression of Bcl-2 was down-regulated, the expression of caspase-12, activated caspase-3 and Bax was up-regulated, and Bcl-2∕Bax ratio was decreased in PNI and UTI groups (P<0. 05). Com-pared with group PNI, AI was significantly decreased, the expression of Bcl-2 was up-regulated, the ex-pression of caspase-12, activated caspase-3 and Bax was down-regulated, and Bcl-2∕Bax ratio was in-creased in group UTI ( P<0. 05) . The pathological changes of the spinal cord were significantly attenuatedin group UTI than in group PNI. Conclusion Ulinastatin can inhibit neuronal apoptosis in the spinal cord after peripheral nerve injury in mice.