Diabetic medicine : a journal of the British Diabetic Association · 2026
The Ligustrum lucidum-derived glycoside specnuezhenide alleviates metabolic-associated fatty liver disease in mice via modulation of gut microbiota and the PPARα signalling pathway.
СтатьяНазвание и аннотация: Перевод в очереди
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.
Gao Kai, Wang Kai, Hao Jikun, Zhang Wei, Zhao Meina, Xu Dong, Tao Xingru, Guo Chao, Li Wangting, Liu Meiyou, Lu Yunyang, Wang Jingwen
Аннотация
BACKGROUND: Metabolic-associated fatty liver disease (MAFLD), particularly advanced metabolic dysfunction-associated steatohepatitis (MASH), leads to irreversible liver damage. Specnuezhenide (SPE), naturally isolated from Ligustrum lucidum Ait, has been demonstrated to exert hepatoprotective effects. However, its functional role and underlying mechanisms in MAFLD remain poorly understood.
PURPOSE: This study investigated the therapeutic effects and potential mechanism of SPE on MAFLD.
METHODS: MAFLD mice induced by high-fat diet (HFD) were employed to assess SPE's therapeutic effects in vivo. The impact of SPE on gut microbiota was analysed by 16S rRNA sequencing. RNA-seq analysis was conducted to uncover SPE's molecular mechanisms. Complementary in vitro investigations utilized FFA-treated HepG2 cells to systematically examine SPE's cellular-level impacts and regulatory pathways.
RESULTS: The results indicated that SPE could improve hepatic steatosis, liver injury and oxidative stress in MAFLD mice. SPE treatment also affected the diversity of gut microbiota and altered their composition by decreasing the Firmicutes/Bacteroidetes (F/B) ratio. The results of 16S rRNA sequencing, RNA-seq and Western blot analysis indicated that the effect of SPE on MAFLD was related to fatty acid beta-oxidation and the PPARα signalling pathway. Moreover, in HepG2 cells, SPE reduced FFA-induced lipid accumulation and oxidative stress, which was dependent on PPARα up-regulation.
CONCLUSION: This is the first study to demonstrate that SPE alleviates MAFLD and is associated with modulation of gut microbiota composition and activation of the PPARα signalling pathway. Our findings suggest a potential link between gut microbiota remodelling and PPARα-mediated fatty acid oxidation, highlighting its potential as a therapeutic candidate for MAFLD.
PURPOSE: This study investigated the therapeutic effects and potential mechanism of SPE on MAFLD.
METHODS: MAFLD mice induced by high-fat diet (HFD) were employed to assess SPE's therapeutic effects in vivo. The impact of SPE on gut microbiota was analysed by 16S rRNA sequencing. RNA-seq analysis was conducted to uncover SPE's molecular mechanisms. Complementary in vitro investigations utilized FFA-treated HepG2 cells to systematically examine SPE's cellular-level impacts and regulatory pathways.
RESULTS: The results indicated that SPE could improve hepatic steatosis, liver injury and oxidative stress in MAFLD mice. SPE treatment also affected the diversity of gut microbiota and altered their composition by decreasing the Firmicutes/Bacteroidetes (F/B) ratio. The results of 16S rRNA sequencing, RNA-seq and Western blot analysis indicated that the effect of SPE on MAFLD was related to fatty acid beta-oxidation and the PPARα signalling pathway. Moreover, in HepG2 cells, SPE reduced FFA-induced lipid accumulation and oxidative stress, which was dependent on PPARα up-regulation.
CONCLUSION: This is the first study to demonstrate that SPE alleviates MAFLD and is associated with modulation of gut microbiota composition and activation of the PPARα signalling pathway. Our findings suggest a potential link between gut microbiota remodelling and PPARα-mediated fatty acid oxidation, highlighting its potential as a therapeutic candidate for MAFLD.