Pakistan journal of pharmaceutical sciences · 2026
Platycodon grandiflorus decoction against lipopolysaccharide (LPS)-induced acute lung injury via Keap1/Nrf2/ARE signaling 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.
Zhang Jia-Yi, Zhang Shu-Ting, Yu Yang, Wang Ju-Tao, Cai Bai-Xiang
Аннотация
BACKGROUND: Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe inflammatory disease with high incidence and mortality rates. The traditional Chinese medicine Platycodon grandiflorus decoction (PGD) exerts protective effects against lipopolysaccharide (LPS)-induced ALI via the PI3K/AKT/NF-κB pathway, but its underlying molecular mechanisms require further elucidation.
OBJECTIVES: This study aimed to investigate the molecular mechanism underlying the protective effects of PGD against LPS-induced ALI.
METHODS: In-vivo experiments employed an LPS-induced ALI mouse model to assess PGD's therapeutic potential. Complementary in-vitro studies examined the molecular mechanisms of PGD-enriched serum using human pulmonary epithelial (A549) and microvascular endothelial (HPMEC) cell lines. Nrf2 involvement in PGD-mediated protection was verified through siRNA-mediated gene silencing and subsequent functional validation.
RESULTS: Both in-vitro and in vivo analyses demonstrated that PGD effectively protects pulmonary tissues from LPS-induced damage. PGD administration notably enhanced Nrf2 nuclear translocation and decreased Keap1 expression at the protein and transcriptional levels, while promoting the expression of HO-1 and NQO1 biomarkers. Notably, Nrf2 gene silencing abolished PGD's therapeutic effects, including its anti-apoptotic properties.
CONCLUSIONS: PGD's therapeutic efficacy in LPS-induced ALI is mediated through modulation of the Keap1/Nrf2/ARE signaling pathway.
OBJECTIVES: This study aimed to investigate the molecular mechanism underlying the protective effects of PGD against LPS-induced ALI.
METHODS: In-vivo experiments employed an LPS-induced ALI mouse model to assess PGD's therapeutic potential. Complementary in-vitro studies examined the molecular mechanisms of PGD-enriched serum using human pulmonary epithelial (A549) and microvascular endothelial (HPMEC) cell lines. Nrf2 involvement in PGD-mediated protection was verified through siRNA-mediated gene silencing and subsequent functional validation.
RESULTS: Both in-vitro and in vivo analyses demonstrated that PGD effectively protects pulmonary tissues from LPS-induced damage. PGD administration notably enhanced Nrf2 nuclear translocation and decreased Keap1 expression at the protein and transcriptional levels, while promoting the expression of HO-1 and NQO1 biomarkers. Notably, Nrf2 gene silencing abolished PGD's therapeutic effects, including its anti-apoptotic properties.
CONCLUSIONS: PGD's therapeutic efficacy in LPS-induced ALI is mediated through modulation of the Keap1/Nrf2/ARE signaling pathway.