Background:The firearm injury of peripheral nerve is one of the most common injuries both in war time and peace time, and its morbidity has a tendency to increase. Although that there have been great progress in the research on peripheral nerve regeneration in the firearm injury, the therapeutic effect is not satisfactory yet, especially in the firearm damage. So it becomes a bothersome problem to the orthopedists. Recent studies indicate that the corresponding spinal cord neurons apoptosis induced by peripheral nerve injury impede nerve regeneration and restoration. However, there are few reports dealing with the characteristics of neuronal apoptosis induced by firearm peripheral nerve wound.Apoptosis involves a complicated cascade events, and a lot of extra- or intracellular death signals can initiate apoptosis program. But the critical factors in the pathogenesis are the caspases families proteolysis enzyme system which may hydrolyze substrates including DNA fragmentation factors (DFF). DFF is composed of two subunits, a 40 kDa caspase-activated nuclease (DFF40) and a 45 kDa inhibitor (DFF45). Cleavage of DFF45 by the complex protease results in the release of DFF40 from its inhibited state and allows nucleosomal DNA degradation, which is the ultimate stage of apoptosis. A novel family of CIDEs (cell death inducing DFF45-like effectors) has been identified recently. They share the conserved amino acid sequence similar to the N-terminal domains in DFF45, as well as in DFF40. Within the CIDEs family, three members, CIDE-A, CIDE-B and CIDE-3 have been identified in human and three members, CIDE-A, CIDE-B and FSP27, have been identified in mouse. While CIDE-B N-terminal has higher affinity to DFF45 than to DFF40. It may sequester DFF45 from the subunit DFF40, then release activated DFF40 and lead to cellular apoptosis, i.e, CIDE-B plays a pivotal role in inducing neuronal apoptosis.Bing the most highly differentiated cell, the neuron body has no regeneration ability; This work was supported by the Major State Basic Research Development Program of China(No.G1999054203)it will loss the substrate needed for peripheral nerve regeneration in case of neuronal apoptosis. So the ways for protecting neurons from apoptosis will significantly rescue peripheral nerve regeneration.To protect neurons from apoptosis, a lot of researches focus on the neurotrophic factors, including their corresponding gene therapy methods. However, the apoptosis relative genes are the intrinsic affecting factors. It is suggested that as the pivotal apoptosis-inducing protein, regulating CIDE-B gene expression with its antisense oligodeoxynucleotides will reduce neurons apoptosis happened in the peripheral nerve injury. And there are no related reports so far.We have investigated and found that the most alterative apoptosis related gene is CIDE-B when rabbit firearm sciatic nerve injury with gene chip technology, and it increased mRNA expression as much as 6.25 times compared to the control group. So there is strong evidence that CIDE-B may play a central role in the cells undergoing apoptosis. The research was carried out from the following three aspects.1. To observe apoptosis features induced by firearm sciatic nerve injury, and explore the different characteristics of neuron apoptosis between firearm and incised peripheral nerve injury, and find a new way to repair peripheral nerve injury.2. To claim the relationship between CIDE-B expression alteration and neurons apoptosis. To elucidate the CIDE-B expression change in the two different kinds of damage to the peripheral nerve.3. To study CIDE-B affecting neuron apoptosis in vitro, to culture rat neurons and induced their apoptosis with scratch injury method, then to use its antisense oligodeoxynucleotides inhibited CIDE-B gene expression to rescue neuron apoptosis, to clarify the relationship of CIDE-B and neuron apoptosis.Method1. Established a model with rabbit sciatic nerve firearm injury used triangle shrapnel as projectile to shoot rabbit sciatic nerve inflic