Animal models of inflammatory pain enable the study of mechanisms linking inflammation and nociception. In this study, we employed the subplantar LPS injection model in mice to explore post-transcriptional regulation of ion channel expression. Consistent with our previous presentations (SAN 2023, 2024) and with earlier findings from the formalin model, LPS induced local inflammation, sex-dependent differences in mechanical sensitivity, and segmental changes in ion channel protein levels accompanied by ERK MAPK phosphorylation. Here we analyzed the mechanisms responsible for these changes. Despite stable mRNA levels in paw tissue and dorsal root ganglia, we detected significant alterations in microRNA miR-485-5p, previously described as a post-transcriptional repressor. These changes paralleled the lumbar L3–L5 gradient observed at the protein level, supporting a microRNA-dependent mechanism for ion channel upregulation in a segment- and sex-specific manner. Together, these results extend previous work by identifying miR-485-5p as a potential mediator of ion channel regulation in acute inflammatory pain, reinforcing the importance of post-transcriptional control in physiopathological models of nociception.