Platelet-Rich Plasma Combined with a Low-Frequency Pulsed Electromagnetic Field Alleviates Sciatic Nerve Injury by Regulating the AMPK/mTOR Signaling Pathway.

Sciatic nerve injury (SNI) is a complex neurological disease, and its occurrence and development are closely related to the apoptosis signaling pathway. The mechanism of platelet-rich plasma (PRP) combined with a low-frequency pulsed electromagnetic field (LFPEMF) regulating apoptosis has not been fully elucidated. The SNI gene chip dataset GSE172064 and data from sham ( = 3) and SNI ( = 3) rats were downloaded from the Gene Expression Omnibus. The differentially expressed genes (DEGs) in the SNI and sham groups were identified with the online tool GEO2R. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases were used to analyze the functional and pathway enrichment of genes in the most important modules. A SNI rat model induced by sciatic nerve crush treatment was established. PRP was injected into the severed end of nerve sutures combined with LFPEMF treatment in SNI rats for 8 weeks. Neuronal regeneration was determined via hematoxylin-eosin (HE) and Nissl staining. The protein levels of the adenosine monophosphate-activated protein (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway and apoptosis markers were detected through quantitative real-time-PCR and immunohistochemistry. This study identified 255 DEGs, including 119 upregulated genes and 136 downregulated genes. GO enrichment and KEGG analyses were performed on the DEGs and revealed functional enrichment mainly in the AMPK/mTOR signaling pathway. Further, the number of Nissl bodies was significantly greater in SNI rats treated with PRP+LFPEMFs than in control rats. The immunohistochemistry results revealed significantly decreased levels of Bax and caspase-3 in the sciatic nerve regions of SNI rats treated with PRP+LFPEMFs. In addition, the Bcl-2 level was increased in SNI rats stimulated with PRP+LFPEMFs. Therefore, this study suggests that PRP combined with LFPEMF treatment inhibits apoptosis in the sciatic nerve during the onset of crush injury by regulating the AMPK/mTOR signaling pathway, thereby promoting neuronal regeneration and potentially serving as a therapeutic strategy for SNI.