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.