Long non‑coding RNA FGD5‑AS1/microRNA‑133a‑3p upregulates aquaporin 1 to decrease the inflammatory response in LPS‑induced sepsis.

Sepsis is a systemic inflammatory response syndrome caused by infections. The present study aimed to investigate the potential mechanism of FGD5‑AS1 in sepsis and lipopolysaccharide (LPS)‑induced inflammatory response. An animal model of sepsis was constructed. LPS was used to induce mice HL‑1 cardiomyocytes to construct a cell model. The association between FGD5‑AS1 and miR‑133a‑3p was investigated through animal and cell models. FGD5‑AS1 overexpression was used to analyze the effect of FGD5‑AS1 on inflammatory reaction. Tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β and IL‑6 levels were detected by enzyme‑linked immunosorbent assay and reverse transcription‑quantitative polymerase chain reaction. The interaction of FGD5‑AS1, miR‑133a‑3p and aquaporin 1 (AQP1) was detected by dual‑luciferase reporter assay and microRNA (miRNA/miR) pull‑down assay. Compared with the control group, the expression of FGD5‑AS1 was decreased and the expression of miR‑133a‑3p was increased in the sepsis group. FGD5‑AS1 overexpression increased LPS‑induced expression of FGD5‑AS1 and AQP1, decreased the expression of miR‑133a‑3p, and inhibited the expression of the inflammatory cytokines, TNF‑α, IL‑6 and IL‑1β. Dual‑luciferase reporter and miRNA pull‑down assays confirmed the interaction of FGD5‑AS1, miR‑133a‑3p and AQP1. These results indicated that FGD5‑AS1 is the competitive endogenous RNA of miR‑133a‑3p on AQP1, and thus FGD5‑AS1 overexpression may be able to inhibit the inflammatory response in sepsis.