Journal of ethnopharmacology · 2025
Active components and mechanisms of Shuganning injection in lessening acetaminophen-induced acute liver injury.
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.
Fu Changli, He Feng, Zhang Li, Li Yaxue, Yang Li, Sun Jia, Chi Mingyan, Gong Zipeng, Zheng Lin, Huang Yong
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Shuganning injection (SGN), a traditional Chinese medicine formula, derived from the traditional Yinchenhao decoction, is commonly used in the clinical management of acute liver injury (ALI). Nonetheless, the specific active ingredients together with mechanisms of action are still uncertain.
AIM OF THE STUDY: To investigate SGN's mechanisms of action and active components against acetaminophen (APAP)-induced ALI.
METHODS: The chemical constituents of SGN were analyzed and identified. The protective properties of SGN were evaluated in HepG2 cells and a rat APAP-induced ALI model. Integrated network pharmacology and metabolomics were employed to investigate the potential active components of SGN and their key biological pathways in alleviating ALI. All active components were screened using pharmacokinetic-pharmacodynamic (PK-PD) modeling, cellular thermal shift assay, biolayer interferometry, and molecular docking. The effects of active components on the alleviation of ALI were verified by molecular biology experiments.
RESULTS: Chemical analysis revealed 21 constituents in SGN. In both a rat model and HepG2 cells, SGN demonstrated protective effects against APAP-induced ALI. SGN could regulate phenylalanine metabolism, arachidonic acid metabolism, biosynthesis of phenylalanine and others, and the tricarboxylic acid cycle in ALI rats. Integrated analysis of metabolomics and network pharmacology data suggested that SGN might alleviate ALI by regulating MAPK signaling pathways, of which ERK and p38 signaling pathways were identified as those most affected by SGN. The active compounds included baicalein, oroxylin A, scutellarin, baicalin, and oroxylin A-7-O-glucuronide. The five active components were found to bind to ERK and p38. The therapeutic effects of active components on ALI were consistent with those of SGN, and their regulation of ERK and p38 signaling in the treatment of ALI was validated experimentally.
CONCLUSION: SGN alleviated ALI by inhibiting ERK and p38 signaling, regulating arachidonic acid and phenylalanine metabolism, among other metabolism, and reducing inflammatory mediator production. The active components were baicalein, oroxylin A, scutellarin, oroxylin A-7-O-glucuronide, and baicalin.
AIM OF THE STUDY: To investigate SGN's mechanisms of action and active components against acetaminophen (APAP)-induced ALI.
METHODS: The chemical constituents of SGN were analyzed and identified. The protective properties of SGN were evaluated in HepG2 cells and a rat APAP-induced ALI model. Integrated network pharmacology and metabolomics were employed to investigate the potential active components of SGN and their key biological pathways in alleviating ALI. All active components were screened using pharmacokinetic-pharmacodynamic (PK-PD) modeling, cellular thermal shift assay, biolayer interferometry, and molecular docking. The effects of active components on the alleviation of ALI were verified by molecular biology experiments.
RESULTS: Chemical analysis revealed 21 constituents in SGN. In both a rat model and HepG2 cells, SGN demonstrated protective effects against APAP-induced ALI. SGN could regulate phenylalanine metabolism, arachidonic acid metabolism, biosynthesis of phenylalanine and others, and the tricarboxylic acid cycle in ALI rats. Integrated analysis of metabolomics and network pharmacology data suggested that SGN might alleviate ALI by regulating MAPK signaling pathways, of which ERK and p38 signaling pathways were identified as those most affected by SGN. The active compounds included baicalein, oroxylin A, scutellarin, baicalin, and oroxylin A-7-O-glucuronide. The five active components were found to bind to ERK and p38. The therapeutic effects of active components on ALI were consistent with those of SGN, and their regulation of ERK and p38 signaling in the treatment of ALI was validated experimentally.
CONCLUSION: SGN alleviated ALI by inhibiting ERK and p38 signaling, regulating arachidonic acid and phenylalanine metabolism, among other metabolism, and reducing inflammatory mediator production. The active components were baicalein, oroxylin A, scutellarin, oroxylin A-7-O-glucuronide, and baicalin.