Mechanism of JAK-STAT signaling pathway inhibitor in post-spinal cord injury

Spinal cord injury (SCI) severely threatened public health. JAK-STAT signaling pathway has been suggested to be involved in the pathogenesis of multiple diseases. The participation of JAK-STAT in SCI, however, requires further studies. We thus investigated the mechanism of JAK-STAT after the occurrence of SCI. A total of 30 SD rats were generated for SCI model, and were randomly divided into group A and group B (N=15 each). Group A rats received the injection of JAK-STAT signaling pathway inhibitor after SCI, while group B received saline injection instead. Motor dyskinesia assay was then performed, followed by HE staining on spinal cord tissues. Ki67 immunohistochemistry was used to detect cell proliferation while immunofluorescent assay detected nuclear status. Cell apoptosis was measured by flow cytometry. Motor dyskinesia assay showed significant retard onset of motor disorder in animals with JAK-STAT inhibitor injection (Group A). Group A also had regular cell morphology with less SCI, and less proliferative cells compared to group B cells (P<0.05). Flow cytometry assay showed larger number of apoptotic cells in JAK-STAT inhibitor treated tissues compared to control cells (P<0.05). JAK-STAT signaling pathway inhibitor may slow the development of SCI via decreasing cell proliferation and enhancing apoptosis.