# Network Pharmacology Combined with Experimental Validation to Investigate the Effects and Mechanisms of Aucubin on Aging-Related Muscle Atrophy

**Authors:** Wenan Li, Kaishu Deng, Mengyue Zhang, Yan Xu, Jingxi Zhang, Qingsheng Liang, Zhiyou Yang, Leigang Jin, Chuanyin Hu, Yun-Tao Zhao

PMC · DOI: 10.3390/ijms26062626 · International Journal of Molecular Sciences · 2025-03-14

## TL;DR

This study explores how Aucubin, a compound from traditional Chinese medicine, helps reduce muscle atrophy related to aging through both computational and experimental methods.

## Contribution

The novel contribution is the integration of network pharmacology with in vitro and in vivo experiments to uncover Aucubin's effects on muscle atrophy and aging.

## Key findings

- Aucubin reduces muscle atrophy-related proteins and improves myotube differentiation in vitro.
- Aucubin attenuates oxidative stress and apoptosis in skeletal muscle cells by modulating key signaling pathways.
- In vivo, Aucubin extends lifespan and improves muscle function in C. elegans.

## Abstract

Aucubin (AU) is one of the main components of the traditional Chinese medicine Eucommia ulmoides Oliv (EU). This study investigated the effects of AU on aging-related skeletal muscle atrophy in vitro and in vivo. The results of network pharmacology revealed the potential therapeutic effects of AU on muscle atrophy. In vitro, AU effectively attenuated D-gal-induced cellular damage, reduced the number of senescence-associated β-galactosidase (SA-β-Gal)-positive cells, down-regulated the expression levels of muscle atrophy-related proteins Atrogin-1 and MuRF1, and improved myotube differentiation, thereby mitigating myotube atrophy. Notably, AU was found to attenuate oxidative stress and apoptosis in skeletal muscle cells by reducing ROS production, regulating Cleaved caspase3 and BAX/Bcl-2 expression in apoptotic pathways, and enhancing Sirt1 and PGC-1α signaling pathways. In vivo studies demonstrated that AU treatment extended the average lifespan of Caenorhabditis elegans (C. elegans), increased locomotor activity, improved body wall muscle mitochondrial content, and alleviated oxidative damage in C. elegans. These findings suggested that AU can ameliorate aging-related muscle atrophy and show significant potential in preventing and treating muscle atrophy.

## Linked entities

- **Proteins:** Fbxo32 (F-box protein 32), TRIM63 (tripartite motif containing 63), BAX (BCL2 associated X, apoptosis regulator), BCL2 (BCL2 apoptosis regulator), SIRT1 (sirtuin 1), PPARGC1A (PPARG coactivator 1 alpha)
- **Chemicals:** Aucubin (PubChem CID 91458), D-gal (PubChem CID 6036)
- **Species:** Caenorhabditis elegans (taxon 6239)

## Full-text entities

- **Genes:** bgal-1 (Beta-galactosidase) [NCBI Gene 188583]
- **Diseases:** Muscle Atrophy (MESH:D009133), myotube atrophy (MESH:D001284)
- **Chemicals:** AU (MESH:C006650), D-gal (-)
- **Species:** Eucommia ulmoides (species) [taxon 4392], Caenorhabditis elegans (species) [taxon 6239]

## Full text

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## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11941843/full.md

## References

62 references — full list in the complete paper: https://tomesphere.com/paper/PMC11941843/full.md

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Source: https://tomesphere.com/paper/PMC11941843