The Degeneration Of Nerve Fiber And Its Mechanism In Spinal Cord After Compession Spinal Cord Injury

Objective: To explore the alterations of nerve fiber degeneration,oligodendrocytes (OLs)apoptosis and MBP expression in spinal cord aftercompression spinal cord injury(CSCI)，so as to clarify the spatial-time ruleand mechanism in the nerve fiber degeneration in CSCI.Method: Seventy adult Sprague-Dawley rats were randomly dividedinto3groups, a normal group（n=30）, a operation group（n=30） and asham operation control group（n=10）.The CSCI model was establishedwith a self-made device in the operation group. The operation process inthe sham operation control group was the same as the operation groupexcept the compression of spinal cord. The segments of compression spinalcord were properly taken at an interval of1,3and7day after operation.HE, Luxol fast blue(LFB),electron microscope（EM）,immunofluorescence(IF) staining, Western blot and terminal deoxynucleotidyl transferasemediated dUTP nick end labeling(TUNEL) were performed to observe thepathological changes of white matters.Result: HE staining showed the edema and spongy degenerationto different degree in the white matter of the injured spinal cord at1,3and7day after compression. EM showed the myelin sheath s-plitted after compression. LFB staining showed that one day after c -ompression the nerve fibers became edema and the extracellular space become became wider and the degeneration of nerve fiber occurred in the white matter; three days after compression, the nerve fiberdegeneration was much more severe in the white matter; seven days after compression a great number of fibers were lost. Compared with the normal and sham operation group, the number of myelinatedfibers w-as markedly decreased in compressed segments of the model group (P<0.05). IF and western blot showed that MBP-positive fibers were degenerated and lost and the expression of MBP was progressively significantly declined after compression, coinciding with LFB staining. TUNEL and APC double staining of IF showed the ce-ll number of oligodendrocyte apoptosis significantly increased after compression.Conclusions: Compressed spinal cord injury may induce nerve fiberstime-dependent demyelination in white matter. MBP expression decreaseand oligodendrocyte apoptosis increase could contribute to the nerve fiberdemyelination.