PAR2 Regulates Glial Scar Formation Via P38MAPK At The Early Stage Of Spinal Cord Injury

Objective To explore the mechanism of PAR2 regulating glial scar formation via p38 MAPK at the early stage of spinal cord injury(SCI) in rats.Methods(1) 72 rats were used to create the model of SCI, and then divided them into model group, p38 MAPK agonist group(Anisomycin group) and p38 MAPK inhibitor group(SB203580 group). Respectively, saline, Anisomycin, SB203580 each 10?L were injected into the damaged spinal cord tissue as interventions of SCI. And set the sham group(24 rats, only received laminectomy) as control group. Detect the experiment indicators on the 1st, 3rd, 7th and 14 th day after SCI, using the BBB scale to evaluate the function of Hind limbs movement, and the expression of GFAP and vimentin were detected by Western blotting and immunofluorescence assay.(2) 72 rats were used to create the model of SCI, and then divide d them into model group, PAR2 agonist group(SLIGRL-NH2 group) an d PAR2 inhibitor group(FSLLRY-NH2 group). Respectively, saline, SLI GRL-NH2, FSLLRY-NH2 each 15?L were injected into the damaged spinal cord tissue as interventions of SCI. And set the sham group(24 r ats, only received laminectomy) as control group. Detect the experiment indicators on the 1st, 3rd, 7th and 14 th day after SCI, using the BBB scale to evaluate the function of Hind limbs movement, and the the exp ression of p-p38 MAPK and GFAP were detected by Western blotting an d double-labelling immunofluorescence.Results(1) On the 14 th day after SCI, the BBB scores of model group was significantly lower than that of sham group(P<0.01). the BBB scores of p38 MAPK inhibitor group was significantly higher than that of model group(P<0.05), but was still lower than that of sham group(P<0.01), and the BBB scores of p38 MAPK agonist group was significantly lower than that of model group(P<0.05). On the 7th and 14 th day after SCI, the expressions of GFAP and vimentin in the model group was significantly higher than that in sham group(P<0.01). the expressions of GFAP and vimentin in p38 MAPK inhibitor group was significantly lower than that in model group(P<0.05), but was still higher than that in sham group(P<0.05), and the expresssions of GFAP and vimentin in p38 MAPK agonist group was significantly higher than that in model group(P<0.05).(2) On the 14 th day after SCI, the BBB scores of model group was significantly lower than that of sham group(P<0.01). the BBB scores of PAR2 inhibitor group was significantly higher than that of model group(P<0.05), but was still lower than that of sham group(P<0.05), and the BBB scores of PAR2 agonist group was significantly lower than that of model group(P<0.05). On the 3rd, 7th and 14 th day after SCI, the expressions of p-p38 MAPK in the model group was significantly higher than that in sham group(P<0.05). the expressions of p-p38 MAPK in PAR2 inhibitor group was significantly lower than that in model group(P<0.05), but was still higher than that in sham group(P<0.05), and the expresssions of p-p38 MAPK in PAR2 agonist group was significantly higher than that in model group(P<0.05). and the expression of p-p38 MAPK reached its maximum at 7th day. On the 7th and 14 th day after SCI, the expressions of GFAP in the model group was significantly higher than that in sham group(P<0.05). the expressions of GFAP in PAR2 inhibitor group was significantly lower than that in model group(P<0.05), but was still higher than that in sham group(P<0.05), and the expresssions of GFAP in PAR2 agonist group was significantly higher than that in model group(P<0.05).Conclusions PAR2 can regulating glial scar formation via p38 MAPK at the early stage of spinal cord injury in rats. inhibit PAR2 or p38 MAPK can reduce the expressions of GFAP and vimentin, lighten glial scar formation after SCI, promote the recovery of neural function.