Frontiers in pharmacology · 2026
Shenze shugan capsules alleviate alcoholic liver injury in association with modulation of the TGF-β/smad4 signaling pathway.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Lu, Gu Qianyu, Tinghe Jia, Sun Zhen, Wang Di, Li Lanzhou, Zang Huiyun, Lin Lijun, Chen Junliang, Wang Chunyue
Аннотация
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.
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.