Ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the MK2/TNF-α pathway

Mitogen-activated protein kinase-activated protein kinase 2 (MK2) and its mediated inflammation are involved in various diseases, including spinal cord injury (SCI). Ultrashortwave (USW) radiation has previously been reported to exert a protective effect on SCI. In the present study, through a series of reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot and immunofluorescence assay, it was found that MK2 and tumor necrosis factor (TNF)-α/interleukin (IL)-1β were elevated in patients with SCI and in H(2)O(2)-treated C8-D1A cells. Through gene level and protein level detection by using of RT-qPCR, western blot, immunofluorescence assay and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling assay, it was demonstrated that USW radiation inhibited the expression of MK2/TNF-α/IL-1β and suppressed the apoptosis of H(2)O(2)-treated C8-D1A cells. Furthermore, it was confirmed that the overexpression of MK2 reversed the protective effect of USW on C8-D1A cells, which indicated that USW achieved its function via regulation of the MK2/TNF-α/IL-1β pathway. Finally, using a constructed in vivo model and a series of RT-qPCR, western blot and IHC detection, it was confirmed that USW suppressed the expression of MK2 to promote functional recovery following SCI. The findings of the present study may provide a novel target and improve on the current understanding of how USW functions in the treatment of SCI.