Reduced SNHG16 promotes sepsis-induced intestinal injury via the miR-15a-5p/AKT3 axis

BACKGROUND: Sepsis is an infection-induced syndrome that is challenging to treat. Sepsis-induced intestinal injury can accelerate sepsis and increase patient mortality. SNHG16 is associated with the progression of sepsis. Therefore, this study explored the role of SNHG16 in sepsis-induced intestinal injury. This study aimed to provide valuable insights into the diagnosis and treatment of sepsis-induced intestinal injury. METHODS: Serum samples were collected from sepsis patients and healthy controls. Sepsis-induced intestinal injury cell model was constructed by treating Caco-2 cells using lipopolysaccharide (LPS). The qRT-PCR was used to measure lncRNA, miRNA, and gene expression. The biological functions of biomolecules on intestinal cells were estimated using flow cytometry, transwell permeability assay and Cell Counting Kit-8 (CCK-8). The oxidative stress status was measured using the antioxidant activity assay. ELISA measured inflammatory cytokines. The mechanism was investigated using dual luciferase reporter assay. RESULTS: In sepsis patients, SNHG16 downregulation discriminated patients with intestinal injury. SNHG16 downregulation led to upregulated expression of miR-15a-5p, which further led to downregulated expression of AKT3. The cell experiments showed that SNHG16 protected intestinal cells from the injury induced by LPS. MiR-15a-5p mediated the damaging impact of SNHG16 downregulation on intestinal cells. MiR-15a-5p affected intestinal cells by downregulating AKT3. CONCLUSION: The downregulation of SNHG16 mediated the injury effect of LPS on intestinal cells by upregulating miR-15a-5p and further targeting AKT3. SNHG16 was a diagnostic biomarker and potential therapeutic target for sepsis-induced intestinal injury.