Upregulation of lncRNA SATB1-AS1 in Serum Promotes Sepsis Progression By Suppressing miR-124-3p and Enhancing Inflammatory Mediator Release.

Sepsis is a life-threatening systemic inflammatory response syndrome. The long non-coding RNA SATB1-AS1 exhibits abnormal expression in blood samples from sepsis patients. This study explores the regulatory role of SATB1-AS1 in sepsis. This study included 58 patients with sepsis and 42 patients with non-septic infections. RT-qPCR was used to detect the expression levels of SATB1-AS1 and miR-124-3p. ROC analysis evaluated the diagnostic value of SATB1-AS1. In an LPS-induced RAW264.7 sepsis model, macrophage differentiation markers, cell proliferation, apoptosis, and inflammatory factor levels were assessed via RT-qPCR, CCK-8 assay, flow cytometry, and ELISA, respectively. DLR and RIP experiments validated the binding relationship between SATB1-AS1 and miR-124-3p. SATB1-AS1 was significantly overexpressed in the serum of sepsis patients, demonstrating good diagnostic value. Conversely, miR-124-3p is downregulated, with both molecules exhibiting targeted binding and negatively correlated expression levels. Knocking down SATB1-AS1 increases miR-124-3p levels, enhances cellular proliferation, reduces apoptosis rates, promotes macrophage M2 polarization, and decreases TNF-α, IL-6, and IL-1β release. SATB1-AS1 holds promise as a novel diagnostic biomarker for sepsis. By binding to miR-124-3p, it promotes the release of inflammatory cytokines from macrophages, thereby exacerbating the pathological progression of sepsis. The SATB1-AS1/miR-124-3p axis may emerge as a new therapeutic target for sepsis.