Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Baitouweng decoction regulates ferroptosis-mediated mitophagy and apoptosis through the SLC7A11/GPX4/FTH1 pathway in ulcerative colitis.
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.
Zhang Liuliang, Zhu Xiaolan, Hu Xiaochao, Feng Hui, Wang Guoqing, Zhang Ying, Wang Xuan, Su Jiayu, Liu Tongtong, Du Xingyue, Zhu Huimin, Gu Limei, Liu E-Hu, Liu Shijia
Аннотация
BACKGROUND: The prevalence of ulcerative colitis (UC) has increased recently, with severe cases potentially progressing to colon cancer. The classic herbal formula Baitouweng Decoction (BTW) has a centuries-long clinical application in UC treatment, but its underlying mechanism remains unclear.
PURPOSE: This study aimed to investigate BTW's efficacy against Dextran Sodium Sulfate (DSS)-induced UC and clarify its mechanisms.
RESULTS: Proteomic analysis identified ferroptosis as a key pathogenic mechanism in UC. In vitro and in vivo experiments showed that BTW reduced UC-associated inflammatory symptoms, normalized the levels of inflammatory factors, and maintained intestinal barrier integrity. Notably, BTW inhibited ferroptosis and restored the antioxidant capacity of the SCL7A11/GSH/GPX4 system, thereby suppressing UC inflammation. Transcriptomic analysis revealed apoptosis and ferroptosis as core pathways for BTW's intervention in UC, with mitophagy serving as a pivotal hub connecting these processes. BTW regulated the PINK1/PARKIN-mediated mitophagy pathway and apoptosis, and this regulation was closely linked to ferroptosis.
CONCLUSION: BTW alleviates UC-related inflammation and intestinal barrier damage by modulating apoptosis, mitophagy, and ferroptosis, while mitigating oxidative stress.
PURPOSE: This study aimed to investigate BTW's efficacy against Dextran Sodium Sulfate (DSS)-induced UC and clarify its mechanisms.
RESULTS: Proteomic analysis identified ferroptosis as a key pathogenic mechanism in UC. In vitro and in vivo experiments showed that BTW reduced UC-associated inflammatory symptoms, normalized the levels of inflammatory factors, and maintained intestinal barrier integrity. Notably, BTW inhibited ferroptosis and restored the antioxidant capacity of the SCL7A11/GSH/GPX4 system, thereby suppressing UC inflammation. Transcriptomic analysis revealed apoptosis and ferroptosis as core pathways for BTW's intervention in UC, with mitophagy serving as a pivotal hub connecting these processes. BTW regulated the PINK1/PARKIN-mediated mitophagy pathway and apoptosis, and this regulation was closely linked to ferroptosis.
CONCLUSION: BTW alleviates UC-related inflammation and intestinal barrier damage by modulating apoptosis, mitophagy, and ferroptosis, while mitigating oxidative stress.