Abstract: Objective To investigate the mechanism of IL-1β in promotingglial scar formation after spinal cord injury. Methods The experimental model of SCI was created by extradural compression of the spinal cord using an aneurysm clip. Rats were randomly divided into model group, sham operation group, IL-1β inhibitor IL-1RA group, IL-1β group and IL-1β+JAK2-STAT3 inhibitor AG490 group, according to different interventions, then were given normal saline, IL-1RA, IL-1β and IL-1β+AG490 every 10μL respectively， sham group received only laminectomy. The motion function of the hindlimbs of rats was measured by Basso Beattie Bresnahan(BBB) scores and the expression of GFAP , vimentin and P-STAT3 were detected by Western blot technique, immunofluorescence assay and immunohistochemistry technique at corresponding time points(at the 8th , 12th hour, 1st, 3rd, 7th and 14th day after SCI）. Results The expression trend of P-STAT3（at the 8th and 12th hour after SCI）, GFAP and vimentin（at the 7th and 14th day afterSCI）was: the expressions of P-STAT3, GFAP and vimentin in the model group were significantly higher compared with the sham group（p<0.01）, the expressions of P-STAT3, GFAP and vimentin in the IL-1RA group were significantly lower compared with the model group（p<0.05） whereas significantly higher compared with the sham group（p<0.05）; the expressions of P-STAT3, GFAP and vimentin in the IL-1β+AG490 group were significantly lower compared with the model group（p<0.05）whereas significantly higher compared with the sham group（p<0.05）, the expressions of P-STAT3, GFAP and vimentin in the IL-1β group weresignificantly higher compared with the model group（p<0.05）. Conclusions IL-1β can improve glial scar formation via JAK2-STAT3 signal, inhibition of IL-1β or JAK2-STAT3 can reduce glial scar formation and promote functional recovery of spinal nerve.

Key words: Key words: spinal cord injury, IL-1β, JAK2-STAT3, GFAP, vimentin