Elucidating the Potential Mechanisms Underlying Distraction Spinal Cord Injury-Associated Neuroinflammation and Apoptosis

• DOI: 10.3389/fcell.2022.839313
• Publication Date: 2022-02-21T10:57:49Z
• Authors: Bo Han; Weishi Liang; Yong Hai; Yuzeng Liu; Yuxiang Chen; Hongtao Ding; Jincai Yang; Peng Yin
• Keywords: distraction spinal cord injury; Cell and Developmental Biology; 03 medical and health sciences; 0302 clinical medicine; inflammatory cytokines; QH301-705.5; apoptosis; Biology (General); porcine model; neuroinflammation

The incidence of distraction spinal cord injury (DSCI), which results from ischemia due to vascular compromise and tract disturbances, remains high. Furthermore, because no ideal animal model that mimics DSCI in clinical settings is available thus far, the related molecular mechanisms underlying remain unclear. Thus, this study aimed establish a porcine investigate neuroinflammation apoptosis these pigs. Before surgery, all pigs were randomly divided into three groups: sham group, osteotomy surgery only; incomplete (IDSCI) complete (CDSCI) plus with motor-evoked potential (MEP) amplitude decreased by approximately 75% 100%, respectively. After modified Tarlov scoring MRC muscle strength used evaluate neurologic function each group. We observed distracted using MRI, then sacrificed. Inflammatory cytokine levels cerebrospinal fluid (CSF) also analyzed. immunofluorescence staining assess neuronal microglial structure astrocyte hyperplasia central lesions (T15). Western blotting was determine expression apoptosis-related proteins. Results showed significantly two groups. T2-MRI relative enhancement at center lesions. H&E Lxol fast blue revealed destroyed normal tissues nerve fiber tracts, exacerbating inflammatory cell infiltration, hyperemia, edema. IL-1β, IL-6, TNF-α increased CSF following DSCI. Immunofluorescence indicated GFAP, Iba-1 DSCI, whereas NeuN reduced. Moreover, promoted protein P53, Bcl-2-associated X (Bax), Caspase-3 tissues, it reduced Bcl-2 expression. This successfully established closely settings, clarified DSCI-associated apoptosis; thus, our findings highlight DSCI-treatment strategies for further establishing suitable drug therapies.