The Expression Of Sonic Hedgehog Signaling Pathway Components After Spinal Cord Injury In Adult Rat

Objective:While the spinal cord tissue subjected to acute injury in adult rat, observed the proliferation and differentiation of the neural precursors. In addition, observed the expression changes of Sonic Hedgehog (SHH) signaling pathway components SHH and Gli-1 molecules which associated with neural precursor cell, investigated the molecular mechanism after spinal cord injury of endogenous neural precursor cell differentiation in adult rats.Methods:A rat model of acute spinal cord injury was used, a random number table method of healthy adult rats was used to divide into normal group, shame-operation group and spinal cord injury each time group, with 5-bromo-2-deoxy-uridine (BrdU) tracers, glial fibrillary acidic protein, myelin basic protein were labeled in neural precursor cells, astrocytes and oligodendrocytes. Different groups of BrdU-positive cells and BrdU/GFAP, BrdU/MBP positive trends doubly labeled cell number were observed by immunofluorescence techniques, to explore the proliferation and differentiation of neural precursor cells after spinal cord injury. In addition, detected the change of SHH signaling pathway components SHH and Gli-1 signal molecules in each group by by real time fluorescent quantitative PCR technique and Western technique, to to explore the regulatory effect of SHH signal pathway in rats after spinal cord injury.Results:In the study of neural precursor cells we found that, a small number of BrdU positive cells and BrdU/GFAP, BrdU/MBP positive cells could be observed in the normal group and the shame group, while the expression of BrdU positive cells and positive double-labeled cells showed a significant increasing trend after spinal cord injury (P<0.05). In addition, for the study of SHH signaling pathway components we found that, the low expression of SHH and Gli-1 protein were observed in normal rats group, the amount of SHH and Gli-1 protein continued to rise after spinal cord injury, which reached a peak at the seventh day, and remained at a high level of expression in twenty-first day after spinal cord injury (P<0.05).Conclusion:The proliferation of precursor cells was significantly increased in rats with spinal cord injury, and differentiated to nerve astrocytes and oligodendrocytes. The expression of SHH signal transduction pathway components were observed in healthy normal rats, after spinal cord injury, SHH and Gli-1 protein expression was significantly increased, its variation was consistent with changes of proliferation of neural precursor cells, which suggested the SHH signal pathway might be involved in the repair regulation of neural cell after spinal cord injury.