# Based on Network Pharmacology and Gut Microbiota to Explore the Underlying Mechanism of Huangqi Gegen Decoction for Treating Metabolic‐Associated Fatty Liver Disease

**Authors:** Linzi Li, Yuxian Zhang, Cong Zhou, Chengxiong Yang, Chunkai Rao, Daoping Zhang, Xu Ai, Xianqiang Shao, Jing Zhou, Yan Yang, Shanshan Lei

PMC · DOI: 10.1002/fsn3.71133 · Food Science & Nutrition · 2025-11-09

## TL;DR

This study explores how Huangqi Gegen Decoction treats fatty liver disease by analyzing its effects on the gut microbiome and key biological pathways.

## Contribution

The study integrates network pharmacology, molecular docking, and gut microbiota analysis to reveal HQGG's mechanisms in treating MAFLD.

## Key findings

- HQGG reduced liver inflammation and oxidative stress in MAFLD rats.
- It modulated gut microbiota and affected the PPAR-γ/NF-κB signaling pathway.
- Key targets like PTGS2, AKT1, and PPARG were identified as involved in HQGG's therapeutic effects.

## Abstract

Huangqi Gegen Decoction (HQGG) is composed of Astragali Radix and Puerariae Lobatae Radix, both of which are recognized as therapeutic agents and edible supplements, and has been reported as a potential treatment for metabolic‐associated fatty liver disease (MAFLD). This study employed a comprehensive approach integrating network pharmacology, molecular docking, in vivo experimentation, and gut microbiota analysis to assess the efficacy of HQGG in treating MAFLD and to explore its molecular mechanisms. The results indicated that HQGG has significantly ameliorated hepatocellular injury, decreased liver inflammation, and oxidative stress in the HFD‐induced MAFLD model rats. The network pharmacology identified 21 bioactive compounds, predicted 238 potential targets, and uncovered that the main active components of HQGG may regulate PTGS2, AKT1, MAPK1, JUN, and PPARG to confer their alleviating effects against MAFLD. HQGG also acted on various signaling pathways to treat MAFLD, such as the AGE‐RAGE signaling pathway in diabetic complications, lipid and atherosclerosis, non‐alcoholic fatty liver disease, and the IL‐17 signaling pathway. The in vivo experiments revealed that HQGG may achieve the effect of anti‐MAFLD by regulating the PPAR‐γ/NF‐κB signaling pathway. The results of gut microbiota analysis showed that HQGG could modulate the species structure and abundance, regulating gut microbiota imbalance of MAFLD rats. Overall, the results disclosed that HQGG can affect bacterial diversity and community structures in the gut and the PPAR‐γ/NF‐κB signaling pathway to treat MAFLD. This study systematically elucidated the potential mechanism of HQGG in treating MAFLD, providing a theoretical basis for the development and application of HQGG as a functional food for preventing MAFLD.

This study employed a comprehensive approach integrating network pharmacology, molecular docking, in vivo experimentation, and gut microbiota analysis to evaluate the efficacy of HQGG in the treatment of MAFLD and to explore its molecular mechanisms. Our findings suggest that HQGG can affect bacterial diversity and community structures in the gut and the PPAR‐γ/NF‐κB signaling pathway to treat MAFLD.

## Linked entities

- **Genes:** PTGS2 (prostaglandin-endoperoxide synthase 2) [NCBI Gene 5743], AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207], MAPK1 (mitogen-activated protein kinase 1) [NCBI Gene 5594], JUN (Jun proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 3725], PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468], PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790]

## Full-text entities

- **Genes:** Pparg (peroxisome proliferator-activated receptor gamma) [NCBI Gene 25664] {aka PPARgamma2}, Ptgs2 (prostaglandin-endoperoxide synthase 2) [NCBI Gene 29527] {aka COX-2, Cox2, PGHS-2, PHS II, Pghs2}, Renbp (renin binding protein) [NCBI Gene 81759], Il17a (interleukin 17A) [NCBI Gene 301289] {aka CTLA-8, IL-17, IL-17A, Il17}, Mapk1 (mitogen activated protein kinase 1) [NCBI Gene 116590] {aka ERK-2, ERT1, Erk2, p42-MAPK}, Akt1 (AKT serine/threonine kinase 1) [NCBI Gene 24185] {aka Akt}, Mok (MOK protein kinase) [NCBI Gene 362787] {aka Rage}, Jun (Jun proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 24516]
- **Diseases:** diabetic complications (MESH:D048909), atherosclerosis (MESH:D050197), non-alcoholic fatty liver disease (MESH:D065626), hepatocellular injury (MESH:D056486), MAFLD (MESH:D005234), liver inflammation (MESH:D007249)
- **Chemicals:** lipid (MESH:D008055)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

11 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12597982/full.md

## References

38 references — full list in the complete paper: https://tomesphere.com/paper/PMC12597982/full.md

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Source: https://tomesphere.com/paper/PMC12597982