# Wanshi Shachong Xiaoji Pills Alleviate Functional Dyspepsia in Mice and Exhibit Lipid-Lowering Effects in a Hepatocyte Steatosis Model

## TL;DR

This study shows that Wanshi Shachong Xiaoji Pills improve digestion issues in mice and reduce liver fat in a lab model, possibly through a key biological pathway.

## Contribution

The novel contribution is demonstrating WSXPs' dual effects on functional dyspepsia and hepatic lipid metabolism, with a proposed mechanism involving the PI3K-Akt pathway.

## Key findings

- WSXPs improved gastrointestinal motility and regulated gut hormones in a functional dyspepsia mouse model.
- WSXPs increased the abundance of beneficial gut bacteria like Akkermansia muciniphila.
- In vitro, WSXPs reduced lipid accumulation and inflammation in hepatocytes and suggested the PI3K-Akt pathway as a potential mechanism.

## Abstract

Objective: To investigate the therapeutic effects and safety profile of Wanshi Shachong Xiaoji Pills (WSXPs) on a functional dyspepsia (FD) mouse model and to preliminarily explore its potential mechanism and impact on associated hepatic metabolism. Methods: An FD model was established in mice using L-arginine. Gastrointestinal motility was assessed by measuring gastric emptying and intestinal propulsion rates. Serum levels of gastrointestinal hormones (MTL, GAS, VIP, CCK) and gut microbiota composition were analyzed. A one-month repeated-dose toxicity study was conducted in normal mice to evaluate safety. The effects of WSXPs on lipid metabolism and inflammation were further examined in a hepatocyte steatosis model in vitro, and network pharmacology was employed to predict potential mechanisms. Results: WSXPs significantly alleviated FD symptoms by improving gastrointestinal motility, bidirectionally regulating gut hormone levels, and increasing the abundance of beneficial bacteria (Akkermansia muciniphila). Long-term administration showed no significant toxicity. In vitro, WSXPS reduced lipid accumulation and inflammation in hepatocytes. Network analysis identified the PI3K-Akt signaling pathway as a potentially central common target, providing a hypothesis for future mechanistic studies. Conclusions: WSXPs effectively improve FD symptoms, modulates gut microbiota, and exhibits potential benefits on hepatic lipid metabolism in vitro, possibly via the PI3K-Akt pathway. This hepatocyte-level finding, combined with its in vivo efficacy in FD, suggests a promising avenue for future research into its potential applications in metabolic-associated conditions. This study provides a scientific foundation for the further development and clinical application of WSXPs in treating FD.