Synchronized dual pulse gastric electrical stimulation improves gastric emptying and activates enteric glial cells via upregulation of GFAP and S100B with different courses of subdiaphragmatic vagotomy in rats.

Previous research and clinical practice have indicated that damage to the vagal nerve may seriously affect gastrointestinal physiological movement behavior. The aim of the current study was to observe the change of gastric motility, as well as enteric glial cells (EGCs) in the stomach with different courses of vagal nerve transection in rats prior to and following synchronized dual pulse gastric electrical stimulation. The gastric emptying rates were measured to assess the gastric motility. The glial markers, containing calcium binding protein (S100B) and glial fibrillary acidic protein (GFAP), were detected by reverse transcription‑quantitative polymerase chain reaction and double‑labeling immunofluorescence analysis. Ultrastructural changes of EGCs were observed using transmission electron microscopy. Gastric emptying was delayed in the terminal vagotomy group, compared with the terminal control group. The effect of long‑term synchronized dual pulse gastric electrical stimulation (SGES) was superior to short‑term SGES in terminal groups. The expression levels of S100B/GFAP were markedly decreased in the terminal vagotomy group compared with the terminal control group. Following short‑term or long‑term SGES, S100B/GFAP gene and protein expression increased in terminal groups. However, long‑term SGES was more effective than short‑term SGES and the difference was statistically significant. Vagal nerve damage leads to gastric motility disorder and weakens the function of EGCs. Therefore, SGES may improve stomach movement behavior and restore the impaired EGCs. The underlying mechanism of the effect remains elusive, but maybe associated with activation of EGCs.