Objective To explore the effect and mechanism of Shenqu Xiaoshi oral liquid on gastrointestinal motility in mice with functional dyspepsia (FD).
Methods Forty KM mice were randomly divided into normal group, low, middle and high dose groups of Shenqu Xiaoshi oral liquid, and the blood routine test and liver and kidney function indexes of the mice were detected. Another 50 KM mice were randomly selected as the normal group. The remaining mice were randomly divided into the model group, low, middle and high dose groups of Shenqu Xiaoshi Oral Liquid, and the FD animal model was established by irregular feeding+L-Arg method; The weight of mice was recorded, the gastric residual rate and intestinal propulsion rate were calculated, the pathological changes of gastric tissues were observed, and the expression of endoplasmic reticulum stress factor inositol demand enzyme 1 (IREl) and tumor necrosis factor receptor related factor 2 (TRAF2) in gastric tissues of mice were detected by real-time fluorescent quantitative PCR (qRT-PCR) and Western blot.
Results White blood cells (WBC), red blood cells (RBC), hemoglobin (HGB), platelets (PLT), lymphocytes (LYM), monocytes (MONO), neutrophils (NEU), aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bile acid (TBA), urea nitrogen (BUN) and creatinine (CRE) were not significantly different among groups (P>0.05); The structure of gastric mucosa, submucosa, muscularis and serosa of mice in each group was clear, and no obvious pathological changes were observed; Compared with the model group, the gastric emptying rate and intestinal propulsion rate in the low, middle and high dose groups of Shenqu Xiaoshi Oral Liquid significantly increased, and the expression of IREl and TRAF2 mRNA and protein in gastric tissue significantly decreased (P<0.05).
Conclusion Shenqu Xiaoshi Oral Liquid has no significant effect on blood routine test, liver and kidney function in normal mice, but can significantly improve gastrointestinal motility in FD mice, which may be related to the down-regulation of the expression of endoplasmic reticulum factors IREl and TRAF2.