# Yiqi Daozhi Formula Reduces the M1 Polarization of Macrophages in Mice With Postoperative Ileus Through Mediating Glycolysis Metabolism

**Authors:** Wang Gang, Zhao Xuan, Wang Ye, Yi Chen, Yu Jing, Zhang Tianle, Shao Mingyue, Tao Yuewei, Jiang Zhiwei

PMC · DOI: 10.1002/iid3.70353 · 2026-02-12

## TL;DR

Yiqi Daozhi Formula helps reduce gut dysfunction after surgery by altering immune cell activity and metabolism in mice.

## Contribution

This study reveals a novel mechanism by which Yiqi Daozhi Formula alleviates postoperative ileus through macrophage polarization and glycolysis regulation.

## Key findings

- Yiqi Daozhi Formula reduces M1 macrophage polarization in mice with postoperative ileus.
- The formula inhibits glycolytic metabolism and the AKT/NF-κB/HIF-1α signaling pathway in macrophages.
- Treatment with Yiqi Daozhi Formula improves gastrointestinal function in a mouse model of postoperative ileus.

## Abstract

Postoperative ileus (POI) represents a disorder of gastrointestinal function following surgical procedures, characterized by a multifaceted etiology. There is an urgent clinical need to search for treatment regimens that improve the therapeutic effect for POI. Current research indicates that Traditional Chinese Medicine (TCM) demonstrates significant efficacy in treating POI. Our research was conducted to delve into the precise therapeutic action of Yiqi Daozhi Formula (YQDZF) in the treatment of POI.

In our study, H&E staining and carmine detection were employed to assess the gastrointestinal functionality in the POI mouse model. ELISA was used to detect levels of MPO, lactic acid, inflammatory factors, and glycolysis. Flow cytometry and qRT‐PCR were employed to examine the levels and expression of macrophage phenotypic markers. Western blotting was used to detect the expression of glycolysis‐ and AKT/NF‐kB/HIF‐1α signaling pathway‐related proteins. Cycloheximide method and MG‐132 method were used to detect the stability of AKT protein.

After making the comparative analysis with the Control group, the POI group mice exhibited pronounced gastrointestinal dysfunction, which was mitigated by treatment with YQDZF. In vivo experiments confirmed that YQDZF treatment markedly decreased M1 macrophage polarization and inhibited the glycolytic pathway. Cellular experiments demonstrated that this therapeutic approach was related to the AKT/NF‐kB/HIF‐1α signaling pathway in macrophages.

YQDZF inhibits the AKT/NF‐kB/HIF‐1α pathway, thereby mediating the M1 polarization of macrophages and the glycolytic metabolism to effectively alleviate the progression of POI.

## Linked entities

- **Proteins:** AKT1 (AKT serine/threonine kinase 1), NFKB1 (nuclear factor kappa B subunit 1), HIF1A (hypoxia inducible factor 1 subunit alpha)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Hif1a (hypoxia inducible factor 1, alpha subunit) [NCBI Gene 15251] {aka HIF-1-alpha, HIF1-alpha, HIF1alpha, MOP1, bHLHe78}, Akt1 (Akt serine/threonine kinase 1) [NCBI Gene 11651] {aka Akt, LTR-akt, PKB, PKB/Akt, PKBalpha, Rac}, Mpo (myeloperoxidase) [NCBI Gene 17523] {aka mKIAA4033}
- **Diseases:** inflammatory (MESH:D007249), disorder of gastrointestinal function (MESH:D005767), POI (MESH:D045823)
- **Chemicals:** Cycloheximide (MESH:D003513), H&amp;E (MESH:D006371), lactic acid (MESH:D019344), carmine (MESH:D002329), MG-132 (MESH:C072553)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12902188/full.md

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Source: https://tomesphere.com/paper/PMC12902188