Journal of ethnopharmacology · 2025
Cortex Dictamni induces cholestatic liver injury via the bile acid-gut-liver axis mediated by FXR signaling pathway in rats.
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.
Xu Xiaomin, Lu Fang, Yu Donghua, Wang Yu, Chen Pingping, Hu Wenkai, Jia Suxia, Wo Jiameixue, Liu Shumin
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Cortex Dictamni (CD) is known for its anti-inflammatory and anti-bacterial properties and is widely used to treat various skin conditions. Despite its therapeutic applications, CD can induce cholestatic liver injury (CLI). However, the underlying mechanism of CD-induced CLI is unclear.
AIM OF THE STUDY: This study aims to explore the potential molecular mechanisms of CD-induced CLI.
MATERIALS AND METHODS: This study used multi-omics approaches, including network toxicology, liver transcriptome sequencing, targeted bile acid (BA) metabolomics, 16S rDNA sequencing, biochemical analysis, and histopathological analysis.
RESULTS: Our results suggest that CD induces liver and intestinal injury, as evidenced by abnormal changes in histopathology and biochemical markers. Network toxicology showed that dictamnine was the primary toxic component of CD-induced CLI. Liver transcriptome analysis showed significant changes in genes related to bile secretion, lipids and oxidative stress. Western blot results showed that CD induced BA metabolism disorder, characterized by significant changes in FXR signaling pathway-related protein levels. Moreover, our results showed that CD induced gut microbiota disturbance and disrupted the intestinal barrier, which may exacerbate CLI via the gut-liver axis.
CONCLUSION: In conclusion, CD exposure is significantly associated with systemic dysregulation of bile acid homeostasis, gut microbiota, and liver function, characterized by FXR signaling suppression, bile acid dysregulation, and gut microbiota alterations.
AIM OF THE STUDY: This study aims to explore the potential molecular mechanisms of CD-induced CLI.
MATERIALS AND METHODS: This study used multi-omics approaches, including network toxicology, liver transcriptome sequencing, targeted bile acid (BA) metabolomics, 16S rDNA sequencing, biochemical analysis, and histopathological analysis.
RESULTS: Our results suggest that CD induces liver and intestinal injury, as evidenced by abnormal changes in histopathology and biochemical markers. Network toxicology showed that dictamnine was the primary toxic component of CD-induced CLI. Liver transcriptome analysis showed significant changes in genes related to bile secretion, lipids and oxidative stress. Western blot results showed that CD induced BA metabolism disorder, characterized by significant changes in FXR signaling pathway-related protein levels. Moreover, our results showed that CD induced gut microbiota disturbance and disrupted the intestinal barrier, which may exacerbate CLI via the gut-liver axis.
CONCLUSION: In conclusion, CD exposure is significantly associated with systemic dysregulation of bile acid homeostasis, gut microbiota, and liver function, characterized by FXR signaling suppression, bile acid dysregulation, and gut microbiota alterations.