| Popis: |
Background Inflammation and tissue infiltration by various immune cells play a significant role in the pathogenesis of neurons suffering the central nervous systems diseases. Although brachial plexus root avulsion (BPRA) leads to dramatic motoneurons (MNs) death and permanent loss of function, however, the crosstalk between cytokines and glial reaction in the spinal cord during injury is far beyond our knowledge. The current study is sought to investigate the alteration of specific cytokine expression patterns of BPRA injured spinal cord during an acute and subacute period.Methods Here, cytokine assay, transmission electron microscopy, and histological staining were utilized to assess the alteration of cytokine network, ultrastructure morphology, as well as glial activation and loss of MNs within two weeks, post-injury on a mouse BPRA model.Results We found that BPRA significantly changed the level of CXCL1, IL12 p70, ICAM1, IP10, MCP-5, MIP1-α and CD93. Moreover, the elevated MIP1-α and CD93 were mostly distributed in MNs of the injured, but few in healthy segments. Also, BPRA significantly induced glial reactions in the ventral horn of injured spinal segments, reflected by robustly elevated the Ionized calcium-binding adaptor molecule 1 (IBA1) and Glial fibrillary acidic protein (GFAP) positive cells. We also observed a severe progressively loss of injured MNs, with a character of both apoptosis and necrosis.Conclusion Overall, these findings suggested that the inflammatory cytokines associated with glial cell proliferation play a vital role in the pathophysiology of MNs death caused by nerve roots injury. |
