| Cauda equina constituted by filum terminale and nerve roots which below conusmedullaris. The functions of cauda equina include conducted the sensation of perineumand saddle area, control urination and defaecation and ankle, knee as well asbulbocavernous reflection. It will lead to low back pain, bilateral or unilateral sciatica,saddle anesthesia, motor weakness, sensory deficit, and urinary incontinence after lesions.Mixter et al.（Mixter and Barr,1934） reported and named it cauda equina syndrome(CES) in the first time in1934. Unlike most of the herniated lumbar discs and spinaldegeneration diseases, patients can can be treated conservatively initially, if without anyclinically improve or experience worsening of neurologic symptoms, they will receiveoperation. While CES require acute surgical decompression. If not, patients may progressto paraplegia and/or permanent neurological dysfunction. It is not fully understood themechanisms of CES. Lesions with CES may caused by mechanical compression of nerves,inflammation, and vascular congestion or ischemia. It is not certain about clinicalimprovement of patients with CES who underwent decompression. It is critical for revealthe mechanisms of CES and look for further therapy beyond surgical decompression.Schwann cells (SCs) wrapped around axons to form myelin, play an important role inthe development, function and regeneration of peripheral nerves. Axonal regeneration andremyelination can be promoted after SCs transplantation, but very few axons could wentthrough the Schwann cells and astrocytes (Astrocytes, ACs) boundary re-enter the thecentral nervous system (CNS). It’s certain that SCs transplantation has been of benefit toCNS injuries, however the effect was limited for the restricted migration of SCs in CNS. Inrecent years, the olfactory ensheathing cell (OEC) transplantation is considered to be oneof the most promising therapies to CNS injuries. OEC are a distinct glial cell type, whichcoexist in peripheral nervous system (PNS) and CNS. OECs share properties with bothSchwann cells and the astrocyte (AC). It can support neurogenesis throughout life in natureenvironment, cytoplasmic processes of OECs wrap the primary olfactory axons, permittingthe tune-over growth of axons into the CNS environment of olfactory bulb (OB). Thefeatures of OECs has been successfully applied to spinal cord injury (SCI). Many studieshave reported that OECs can conduct axonal growth after transplantation of CNS injuries,permitting long-term outgrowth so as to promote recovery. Neurotrophic factor gene-modified OEC transplantation in rats can significantly promote corticospinal tractregeneration after SCI. There were no reports about OEC transplantation in CES.Early studies indicated that the cauda equina lesions lead to neuronal apoptosis indorsal root ganglion (DRG) and posterior horn of the spinal cord, brain-derivedneurotrophic factor (BDNF) could promote function recovery in light and moderate lesionsof the cauda equina, while ineffective on severe injury. Further studies on the effects ofOEG following implantation in the cauda equina after various injury degrees of lesion areneeded to find out whether or not it will result in functional recovery, promoting nerveregeneration and remyelination.In the present study, we used in vivo models to test the effect of functional recovery ofcauda equina lesions after OEC transplantation. The contents and results are following:1. Primary cultured olfactory ensheathing cells from the olfactory nerve layer,labeling specificity markers P75NTR and S100with antibody, Hoechst33342labelingnucleus. Purity of of cultured OEC was more than95%according to the consideration ofthe formula. The purity is able to meet the needs of this experiment2. Successful creation of the cauda equina compression model in rats by placed siliconblock (length:10mm, width:1mm, thickness:0.8mm) into the epidural space under theL4-5vertebra to compress7days. Evaluate compression injury model in rats throughbehavioral experiments, such as the open-field BBB scoring system, tail flick latency, aswell as cauda equina nerve immunohistochemistry demyelination byimmunohistochemistry assessment.3. After7days of compression on cauda equina, the silicon block was removed. Ratswere randomly divided into three groups: PBS group (after7days compression, processdecompression operation and injected PBS), OECs group (after7days compression,process decompression operation and injected OECs).4. After the transplantation, GFP fluorescence intensity of cell suspension of the siteof compression was detected by flow cytometry. Fluorescence intensity of OECstransplantation group was higher than the background value of the wild-type organizationswithin2weeks. These indicated that OECs could be found in the site of injury for2weeks.5. The open-field BBB scoring system was performed by two researchersindependently, who familiar with the rules. Scores were recorded on the first and third dayafter operation, and one time per week until4weeks after operation. Tail flick latency(TFL) measures the rats to move its tail out of the light at the same time points. Significant difference was examined by the Mann-Whitney U test at P <0.05. OEC-injected ratsshowed no significant improvement of BBB scores and TFL as compared to thePBS-injected rats within4weeks (P>0.05).Conclusion：Remyelination of cauda equian of rats was promoted after OECstransplantation, which originated from olfactory bulb. MBP expression levels of the OECsgroup was higher than that of the PBS group at2-3weeks. OECs transplantation may bethrough cell-cell interactions, such as the secretion of neurotrophic factor, activated SCsand clear necrotic tissue to protection cauda equina when it was demyelination. However,animals under OECs transplantation didn’t get better function recovery. Futuretranslational studies are expected to find the way to access functional recovery in OECstransplantation for cauda euqina compression injury. |
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