| Research BackgroundThe spinal cord injury (SCI) rate is 15-40 per million annual year in each country. The more economic development, the more incidences in spinal cord injury. The results of which is deformity due to the SCI. It remains hot recently on basic and clinic research that how we can promote the function of SCI.It is well known that decompression is one of the effective operations for the spinal cord injury followed by fracture. But the mechanism remains unclear.The pathobiologic progress of SCI is being clarified step by step, the cause of which is classified by primary injury and secondary injury. The prognosis of SCI is the interactive effect of these two injuries. The secondary injury is a series of molecular biologic reaction caused by the primary injury, while the causes of the secondary injury are cellular toxity, free radical injury, inflammation, cell apoptosis, etc. the progress is reversible that there is the opportunity for us to treat the SCI.Apopcell is specified by nucleus chromatin condensation, nucleus shrinks and DNA fragments. TUNEL (Terminal deoxynucleotidyl-transferase-mediated deoxyuridine triophosphate-biotin nick end labeling) is common method due to checking apoptosis. The regulator of apoptosis is composed of bcl-2 family. Some of them promote apoptosis such as bax and bad, while the other restrain apoptosis such as bcl-2, bcl-Xl, the relative level of these proteins makes cells die or live. The bad or bax proteins act by caspases, the cysteine proteinase. It is certificated that apoptosis is controlled by these proteins.It is not ever reported before for the regulation of apoptosis after continuous compression and the relationship between the decompression and apoptosis. We try to make it clear what is the relationship between decompression and apoptosis and what is the mechanism of decompression.Methods1. The experiment model is completed by putting a screw on the dura after laminectomy of T10. 78 adult SD rats (from experiment animal ceter of Medical College, Zhejiang University), 300-400 gram, male, is randomly classified into 4 groups including decompression after 6 hours, decompression after 24 hours, continuous cmpression group and the control. Each group was executed at 1 day, 3days, 7days and 30 days after decompression.2. Each rat was scored at 1 day, 3days, 7days and 30 days after decompression by BBB(Basso-Beattie-Bresnahan locomotive rating scale) system.3. Histopathology:After anesthesia with phentobarbital (50mg/kg, i.p), the rat was perfused intracardiovascularly by normal saline in 15 minutes followed by 4% formaldehyde 30 minutes. And then 15 milimetre spinal cord cetered at the lesion was removed carefully and immersed in 4% formaldehyde in 4 centigrade freezer for postfixation for 24-48 hours. The specimen was cut into 3 parts which are rostral-, lesion and caudal part by paraffin en bloc.4 m transect slice was made to H.E, TUNEL, Caspase-3 antibody, bcl-2/bax.Statistic method1, SPSS 11.0 for Windows .2 , One way ANOVA, there is difference whin groups when P < 0.05.3 , Interactive graphs for analysis 鈥?ResultsThe BBB scoreThere is prominent difference between 6 hour group and continuous group at 3 day, 7 day, 30 day after decompression, while there is prominent difference within 6 hour group, 24 hour group and continuous group (p<0.05).TUNELThe apoptosis cells were counted in OLYMPUS BX51 light microscope each by each according to anterior column (AC), lateral column (LC), posterior column (PC), anterior horn (AH, AH1 is neuron, AH2 is gliocell), posterior horn (PH, PHI is neuron, PH2 is gliocell).It appears apoptosis cell in each group 1 day after decompression, and then the apoptosis cell develops, the high level of the apoptosis cell of 6 hour group is in 7 day, while that of the other two groups is in 3 day after decompression. There is apoptosis cell in 30 day after decompression.At rostral segment, 1 day after decompression the number of apopcell of the continuous group is bi...
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