Shenze shugan capsules alleviate alcoholic liver injury in association with modulation of the TGF-β/smad4 signaling pathway
- 1Engineering Research Center of Chinese Ministry of Education for Edible and Medicinal Fungi, Jilin Agricultural University , ,
- 2Jilin Aodong Shihang Pharmaceutical Co., Ltd. , ,
- 3Jilin Aodong Pharmaceutical Group Yanji Co., Ltd. , ,
Abstract
Background: Alcohol-associated liver disease (ALD) represents a major contributor to liver fibrosis globally, and current therapeutic options remain inadequate. The TGF-β/Smad4 cascade is critically involved in alcohol-evoked activation of hepatic stellate cells and subsequent extracellular matrix accumulation. Although Shenze Shugan capsule (SZSG) has been clinically used for non-alcoholic steatohepatitis, its efficacy and mechanisms in ALD are unclear. This study aimed to explore how SZSG exerts protective effects against alcohol-triggered liver injury and the underlying mechanisms.
Methods: Both acute and chronic ALD mouse models were established to assess liver injury, fibrosis, inflammation, gut microbiota composition, and serum metabolomic profiles.
Results: SZSG treatment markedly attenuated hepatic steatosis, fibrosis, and inflammation, as evidenced by reductions in lipid accumulation, collagen deposition, and pro-inflammatory cytokine levels. Concurrently, it reshaped the gut microbiota and restored metabolites dysregulated by alcohol exposure. These beneficial effects appear to involve modulation of the TGF-β/Smad4 signaling pathway and its downstream effectors, α-SMA and Collagen I.
Conclusion: Collectively, our findings suggest that SZSG combats ALD by simultaneously modulating the TGF-β/Smad4 signaling axis and preserving gut-liver homeostasis, thereby representing a promising multi-target therapeutic candidate.
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BibTeX
@article{wang2026shenze,
title = {{Shenze shugan capsules alleviate alcoholic liver injury in association with modulation of the TGF-β/smad4 signaling pathway}},
author = {Lu Wang and Qianyu Gu and Jia Tinghe and Zhen Sun and Di Wang and Lanzhou Li and Huiyun Zang and Lijun Lin and Junliang Chen and Chunyue Wang},
journal = {Frontiers in pharmacology},
year = {2026},
month = oct,
doi = {10.3389/fphar.2026.1942947},
url = {https://europepmc.org/article/PMC/PMC13671995},
note = {CC BY},
}
RIS
TY - JOUR
TI - Shenze shugan capsules alleviate alcoholic liver injury in association with modulation of the TGF-β/smad4 signaling pathway
AU - Lu Wang
AU - Qianyu Gu
AU - Jia Tinghe
AU - Zhen Sun
AU - Di Wang
AU - Lanzhou Li
AU - Huiyun Zang
AU - Lijun Lin
AU - Junliang Chen
AU - Chunyue Wang
PY - 2026
DA - 2026/10/02
JO - Frontiers in pharmacology
DO - 10.3389/fphar.2026.1942947
UR - https://europepmc.org/article/PMC/PMC13671995
AB - Background: Alcohol-associated liver disease (ALD) represents a major contributor to liver fibrosis globally, and current therapeutic options remain inadequate. The TGF-β/Smad4 cascade is critically involved in alcohol-evoked activation of hepatic stellate cells and subsequent extracellular matrix accumulation. Although Shenze Shugan capsule (SZSG) has been clinically used for non-alcoholic steatohepatitis, its efficacy and mechanisms in ALD are unclear. This study aimed to explore how SZSG exerts protective effects against alcohol-triggered liver injury and the underlying mechanisms. Methods: Both acute and chronic ALD mouse models were established to assess liver injury, fibrosis, inflammation, gut microbiota composition, and serum metabolomic profiles. Results: SZSG treatment markedly attenuated hepatic steatosis, fibrosis, and inflammation, as evidenced by reductions in lipid accumulation, collagen deposition, and pro-inflammatory cytokine levels. Concurrently, it reshaped the gut microbiota and restored metabolites dysregulated by alcohol exposure. These beneficial effects appear to involve modulation of the TGF-β/Smad4 signaling pathway and its downstream effectors, α-SMA and Collagen I. Conclusion: Collectively, our findings suggest that SZSG combats ALD by simultaneously modulating the TGF-β/Smad4 signaling axis and preserving gut-liver homeostasis, thereby representing a promising multi-target therapeutic candidate.
SN - 1663-9812
ER -