中文摘要：

Evidence suggested that glycogen synthase kinase-3β(GSK-3β) is involved in Nogo-66 inhibiting axonal regeneration in vitro, but its effect in vivo was poorly understood. We showed that stereotactic injection of sh RNA GSK-3β-adeno associated virus(GSK-3β-AAV) diminished syringomyelia and promoted axonal regeneration after spinal cord injury(SCI), using stereotactic injection of sh RNA GSK-3β-AAV(tested with Western blotting and RT-PCR) into the sensorimotor cortex of rats with SCI and by the detection of biotin dextran amine(BDA)-labeled axonal regeneration. We also determined the right position to inject into the sensorimotor cortex. Our findings consolidate the hypothesis that downregulation of GSK-3β promotes axonal regeneration after SCI.

英文摘要：

Evidence suggested that glycogen synthase kinase-3β（GSK-3β） is involved in Nogo-66 inhibiting axonal regeneration in vitro, but its effect in vivo was poorly understood. We showed that stereotactic injection of sh RNA GSK-3β-adeno associated virus（GSK-3β-AAV） diminished syringomyelia and promoted axonal regeneration after spinal cord injury（SCI）, using stereotactic injection of sh RNA GSK-3β-AAV（tested with Western blotting and RT-PCR） into the sensorimotor cortex of rats with SCI and by the detection of biotin dextran amine（BDA）-labeled axonal regeneration. We also determined the right position to inject into the sensorimotor cortex. Our findings consolidate the hypothesis that downregulation of GSK-3β promotes axonal regeneration after SCI.