Conclusion
EES significantly improved gastric emptying by regulating gastrointestinal hormone excretion and c-Kit/SCF signaling pathway. Our study provides a pharmacological basis for the use of the EES in the treatment of DGP. However, the detailed molecular mechanism remains to be clarified.
Methods
Rats were divided into six groups: normal control group (NC), diabetic gastroparesis model group (DGP), low, medium, and high dose of EES groups (LES, MES, and HES, respectively), and metoclopramide positive group (MPG). DGP rats were induced by streptozotocin (STZ) combined with a high-sugar-high-fat diet. The gastric emptying was measured by the phenol red labeling method. Enzyme-linked immunosorbent assay (ELISA) was employed to determine the concentrations of serum ghrelin, gastrin (GAS), somatostatin (SS), and vasoactive intestinal peptide (VIP). The expressions of c-Kit and its natural ligand stem cell factor (SCF) in gastric tissues were determined by Western blot and immunofluorescence.
Results
Gastric emptying rate increased in a different degree after intervention by EES, among which MES and HES groups showed a significant effect (compared with DGP, P<0.01) and the HES group was equivalent to the MPG group; serum ghrelin and content of serum GAS increased while SS and VIP decreased (compared with the DGP group, P<0.05 or P<0.01); c-Kit and SCF protein expressions in gastric tissue increased (compared with DGP group, P<0.05 or P<0.01).