Effects of β‑hydroxybutyric acid and ghrelin on the motility and inflammation of gastric antral smooth muscle cells involving the regulation of growth hormone secretagogue receptor

Ghrelin is an orexigenic hormone that is produced by gastric cells. Ghrelin stimulates food intake and increases gastric movement. In rat model, injected β‑hydroxybutyric acid (β‑HB) leads to a decrease in body weight. It has been reported that patients with gastric erosions are slower to evacuate the stomach. The aim of the present study was to investigate the effects of ghrelin and β‑HB on motility and inflammation in rat gastric antral smooth muscle cells (GASMCs). GASMCs were extracted from rat gastric antrum. Cell viability was determined using the Cell Counting Kit‑8 assay. A Reactive Oxygen Species (ROS) assay kit was used to analyze the levels of ROS using flow cytometry. Protein levels were determined using western blotting, and the expression levels of mRNAs were evaluated using reverse transcription‑quantitative PCR. β‑HB inhibited the expression of Myosin regulatory LIGHT polypeptide 9 (MYL9), Myosin light chain kinase (MLCK), transforming protein RhoA (RhoA), Rho‑associated protein kinase‑1 (ROCK‑1) and growth hormone secretagogue receptor (GHS‑R). By contrast, ghrelin increased the expression of MYL9, MLCK, RhoA, ROCK‑1 and GHS‑R in β‑HB‑treated GASMCs. β‑HB increased the levels of tumor necrosis factor (TNF)‑α, interleukin (IL)‑6 and ROS, and decreased the levels of manganese (Mn) superoxide dismutase (SOD), copper/zinc (Cu/Zn)SOD and catalase. Ghrelin decreased the expression of TNF‑α, IL‑6, ROS and catalase, whereas ghrelin promoted the expression of MnSOD and Cu/ZnSOD in β‑HB‑treated GASMCs. Short interfering RNA targeting GHS‑R inhibited the expression of MYL9, MLCK, RhoA and ROCK‑1, and increased the levels of TNF‑α, IL‑6 and ROS in β‑HB‑treated or ghrelin‑treated GASMCs. The present study provided preliminary evidence that β‑HB inhibits the motility of GASMCs and promotes inflammation in GASMCs, whereas ghrelin decreases these effects. GHS‑R acted as a primary regulator of motility and inflammation in GASMCs treated with β‑HB and ghrelin.