Oral diseases · 2018
Exogenous hydrogen sulfide inhibits oral mucosal wound-induced macrophage activation via the NF-κB 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.
Zhuang R, Guo L, Du J, Wang S, Li J, Liu Y
Аннотация
OBJECTIVE: This study includes exploring (i) the production of endogenous hydrogen sulfide (H2 S) after mucosal wound generation and (ii) the role of compensating the change in H2 S level postmucosal wound generation.
METHODS AND MATERIALS: A mucosal wound model was established in female C57BL/6J mice. Wound tissues were collected to examine the change in the endogenous H2 S level. To examine the effect of decreased H2 S, GYY4137 was intraperitoneally injected into mice at 50 mg kg-1 day-1 before mucosal wounding to compensate for the decreased endogenous H2 S. Finally, we confirmed the role of GYY4137 in inhibiting the M1 phenotype macrophage activation induced by LPS in peritoneal macrophages and RAW264.7.
RESULTS: The production of endogenous H2 S and the expression of cystathionine b-synthase and cystathionine g-lyase in vivo were reduced significantly in early stage after wound. GYY4137 significantly inhibited the activation of the M1 phenotype induced by mucosal wound inflammation in vivo and LPS in vitro. Finally, we confirmed that GYY4137 inhibited iNOS expression via the NF-κB signaling pathway.
CONCLUSION: The exogenous H2 S donor GYY4137 compensated for the reduced endogenous H2 S postmucosal wound generation and inhibited the induced M1 macrophage activation. Thus, appropriate H2 S supplementation may aid in controlling inflammation associated with mucosal wounds.
METHODS AND MATERIALS: A mucosal wound model was established in female C57BL/6J mice. Wound tissues were collected to examine the change in the endogenous H2 S level. To examine the effect of decreased H2 S, GYY4137 was intraperitoneally injected into mice at 50 mg kg-1 day-1 before mucosal wounding to compensate for the decreased endogenous H2 S. Finally, we confirmed the role of GYY4137 in inhibiting the M1 phenotype macrophage activation induced by LPS in peritoneal macrophages and RAW264.7.
RESULTS: The production of endogenous H2 S and the expression of cystathionine b-synthase and cystathionine g-lyase in vivo were reduced significantly in early stage after wound. GYY4137 significantly inhibited the activation of the M1 phenotype induced by mucosal wound inflammation in vivo and LPS in vitro. Finally, we confirmed that GYY4137 inhibited iNOS expression via the NF-κB signaling pathway.
CONCLUSION: The exogenous H2 S donor GYY4137 compensated for the reduced endogenous H2 S postmucosal wound generation and inhibited the induced M1 macrophage activation. Thus, appropriate H2 S supplementation may aid in controlling inflammation associated with mucosal wounds.