English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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 H2O2‑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 H2O2‑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.

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