miR-1224-5p modulates SND1 expression and correlates with NF-κB signaling in alleviating systemic inflammatory response syndrome following total hip arthroplasty

Total hip arthroplasty (THA) is recognized as the optimal treatment for femoral neck fracture (FNF). However, the inflammatory response triggered by surgical trauma cannot be ignored. This study primarily investigated the functions and mechanisms of miR-1224-5p in systemic inflammatory response syndrome (SIRS) following THA. The study comprised 300 FNF patients undergoing THA, of whom 128 developed SIRS after THA. RT-qPCR was employed to quantify miR-1224-5p and SND1 levels. Cell viability was assessed via CCK-8 assay, while inflammatory markers were detected using ELISA kits. The NF-κB pathway activation was evaluated by Western blotting. The binding interaction was validated through luciferase activity and RIP assays. Serum miR-1224-5p levels were decreased in patients with SIRS after THA compared with the non-SIRS group. Lipopolysaccharide (LPS) treatment impaired THP‑1 macrophage viability, activated inflammatory responses, and activated the NF-κB signaling pathway. miR-1224-5p mimic improved LPS-induced THP‑1 cell function, while miR-1224-5p inhibitor further suppressed the biological functions of the cells. Mechanistically, SND1 was identified as a direct downstream target of miR-1224-5p, and up-regulation of SND1 partially reversed the protective properties of miR-1224-5p on THP-1 cells. miR-1224-5p may be associated with the post-THA inflammatory response, potentially involving SND1, accompanied by alterations in the NF-κB pathway. However, a strict linear axis or target dependence cannot be concluded from the current data. miR-1224-5p is expected to be a promising biomarker and therapeutic candidate for further investigation. Not applicable.