Pulsed Radiofrequency Alleviates Acute Soft Tissue Injury in Rats by Regulating the TNF/mTOR Signaling Pathway

<b><i>Objective:</i></b> Acute traumatic muscle injuries are common and result in substantial loss of time and risk of recurrence. Pulsed radiofrequency (PR) is a strategy that has been gradually adopted for treating muscle injuries in clinical practice. However, the molecular mechanism underlying its therapeutic effects is currently unclear. <b><i>Materials and Methods:</i></b> In this study, we screened the gene expression profiles of rats with muscle contusion obtained from the online dataset GSE162565. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of the differentially expressed genes were conducted. Further, we established an acute soft tissue injury (ASTI) rat model and applied PR treatment. Muscle swelling rate analysis, malondialdehyde (MAD) and superoxide dismutase (SOD) content, inflammatory cytokine release, and hematoxylin and eosin staining of the gastrocnemius muscles of ASTI and ASTI + PR rats were performed, and the results were compared with those of control rats. Further, we evaluated the gene expression of <i>Ccl1</i>, <i>interleukin-6</i> (<i>IL-6</i>), <i>nuclear factor-kappa-B-inhibitor alpha</i> (<i>Nfkbia</i>), <i>Akt1</i>, <i>Jun</i>, <i>Fos</i>, and <i>Caps3</i> in the model and PR-treated groups, all of which are key genes in the tumor necrosis factor (TNF)/mechanistic target of rapamycin (mTOR) signaling pathway according to the KEGG analysis. <b><i>Results:</i></b> The results revealed that 52 genes involved in the TNF/mTOR signaling pathway were closely associated with ASTI progression in rats. PR treatment significantly reduced the malondialdehyde content but increased the SOD content in ASTI model rat muscles, efficiently alleviated muscle contusions and reduced TNF-α and IL-1β production. Moreover, PR treatment significantly decreased <i>Ccl1</i>, <i>IL-6</i>, and <i>Nfkbia</i> expression but increased <i>Akt1</i>, <i>Jun</i>, <i>Fos</i>, and <i>Caps3</i> levels in ASTI models. These data indicate that PR alleviated ASTI in rats by mediating redox homeostasis and the inflammatory response, which might be modulated by the TNF/mTOR signaling pathway. <b><i>Conclusions:</i></b> Thus, this study contributes to the understanding of ASTI progression and provides more substantial information about the genetic mechanism underlying the therapeutic effects of PR on ASTI.