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.