The study aimed to determine the effects of protease-activated
receptor-2 (PAR-2) on glial scar formation after spinal cord injury
(SCI) in Sprague–Dawley (SD) rats and the underlying
mechanisms. Rivlin and Tator’s acute extradural clip compression
injury (CCI) model of severe SCI was established in this study.
Animals were divided into four groups: 1) sham group
(laminectomy only); 2) model group, treated with normal saline;
3) PAR-2 inhibitor group; 4) PAR-2 activator group. Enhanced
GFAP and vimentin expression were the markers of glial scar
formation. To determine whether JNK was involved in the effects
of PAR-2 on GFAP and vimentin expression, we administered
anisomycin (a JNK activator) in the presence of PAR-2 inhibitor
and SP600125 (a JNK inhibitor) in the presence of PAR-2
activator. At 1, 7, 14 and 28 day after SCI, Basso, Beattie, and
Bresnahan (BBB) locomotor score test was used to assess the
locomotor functional recovery; immunofluorescence and western
blot analysis were used to assess the expression level of GFAP,
vimentin and p-JNK. Double immunofluorescence staining with
GFAP and tubulin β was used to assess the glial scar formation
and the remaining neurons. Results suggested that PAR-2 is
involved in glial scar formation and reduces neurons residues
which can cause a further worsening in the functional outcomes
after SCI via JNK signaling. Therefore, it may be effective to
target PAR-2 in the treatment of SCI.