Electroacupuncture ameliorates gastrointestinal motility and modulates PLC-IP3 signaling in a rat model of functional dyspepsia

Objective: The aim of this study was to determine whether electroacupuncture (EA) modulates the phospholipase C—inositol-1,4,5-trisphosphate (PLC-IP3) pathway and platelet-derived growth factor receptor (PDGFR)α + cells in a rat model of functional dyspepsia (FD) characterized by gastrointestinal (GI) motor dysfunction. Methods: Forty Sprague-Dawley (SD) rats were allocated into five groups: control, model, EA, U73122 and U73122 + EA groups (n = 8 each). All groups except the control group underwent a multifactorial method to induce FD. The EA group received EA, the U73122 group received the PLC inhibitor U73122, and the U73122 + EA group received U73122 prior to EA. The control and model groups received no interventions. After 10 days of treatment, behavioral and GI motility tests were conducted. Gastric antrum tissues were analyzed post-euthanasia to determine PDGFRα, PLC, phosphorylated ( P )-PLC, and IP3 expression and co-localization using Western blotting, RT-qPCR and immunofluorescence. Electron microscopy was used to examine gastric antrum gap junctions (GJs) and PDGFRα + cells. Results: The FD model rats displayed reduced activity, weight gain and food intake, with altered GI motility, widened gastric antrum GJs and decreased mRNA/protein expression of PDGFRα, PLC, P -PLC and IP3. Post-EA, rats showed improved weight gain, food intake, GI motility and mRNA/protein expression, as well as normal GJs. The U73122 group failed to demonstrate significant improvements in motility or PDGFRα + cell morphology, with lower protein/mRNA expression of key pathway intermediates than the EA group. Conclusion: EA enhances GI function in FD rats by activating the PDGFRα + cell-associated PLC-IP3 pathway, demonstrating potential as a therapeutic target for FD.