Journal of ginseng research · 2025
Gintonin enhances epithelial barrier function by activating NRF2 pathway in radiation-induced intestinal injury.
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.
Jang Hyosun, Kim Hyewon, Oh Su-Hyun, Son Yeonghoon, Lee Rami, Nah Seung-Yeol, Lee Hae-June
Аннотация
BACKGROUND: Because the intestine is a radio-sensitive organ in the body, and radiation-induced intestinal injury is a major clinical problem associated with radiotherapy or radiological accidents. Dysfunction of the epithelial barrier leads to bacterial translocation to other organs, resulting in severe inflammation. Recent findings suggest that gintonin (GT) suppresses oxidative stress and inflammation in neuroinflammatory diseases.
PURPOSE: This study objected to elucidate the mitigating effects of GT on radiation-induced intestinal injury.
METHODS: The therapeutic effects of GT were assessed in a mouse model of radiation-induced intestinal injury using histological, immunohistochemical, and real-time PCR. Additionally, the direct effects of GT and NF-E2-related factor 2 (NRF2) activators on radiation-induced epithelial damage were assessed using Caco-2 cell monolayers.
RESULTS: GT treatment reversed radiation-induced body weight loss, attenuated intestinal damage, and inhibited inflammatory response by reducing inflammatory cell infiltration and cytokine expression in the intestines of mice. Additionally, GT treatment activated NRF2 and ameliorated intestinal barrier damage. In vitro experiments showed that GT treatment affected epithelial permeability and intercellular junction expression in Caco-2 cell monolayers under irradiated conditions. Moreover, treatment with NRF2 activator improved epithelial permeability, improved the expression of intercellular junctions in irradiated epithelial cells, and attenuated radiation-induced intestinal injury in a mouse model.
CONCLUSION: GT maintains epithelial integrity by activating NRF2-mediated antioxidant activity in radiation-induced intestinal epithelial damage of mice. Overall, these results suggest that GT could be a novel therapeutic agent for radiation-induced intestinal damage.
PURPOSE: This study objected to elucidate the mitigating effects of GT on radiation-induced intestinal injury.
METHODS: The therapeutic effects of GT were assessed in a mouse model of radiation-induced intestinal injury using histological, immunohistochemical, and real-time PCR. Additionally, the direct effects of GT and NF-E2-related factor 2 (NRF2) activators on radiation-induced epithelial damage were assessed using Caco-2 cell monolayers.
RESULTS: GT treatment reversed radiation-induced body weight loss, attenuated intestinal damage, and inhibited inflammatory response by reducing inflammatory cell infiltration and cytokine expression in the intestines of mice. Additionally, GT treatment activated NRF2 and ameliorated intestinal barrier damage. In vitro experiments showed that GT treatment affected epithelial permeability and intercellular junction expression in Caco-2 cell monolayers under irradiated conditions. Moreover, treatment with NRF2 activator improved epithelial permeability, improved the expression of intercellular junctions in irradiated epithelial cells, and attenuated radiation-induced intestinal injury in a mouse model.
CONCLUSION: GT maintains epithelial integrity by activating NRF2-mediated antioxidant activity in radiation-induced intestinal epithelial damage of mice. Overall, these results suggest that GT could be a novel therapeutic agent for radiation-induced intestinal damage.