Emodin protects against severe acute pancreatitis-associated acute lung injury by activating Nrf2/HO-1/GPX4 signal and inhibiting ferroptosis in vivo and in vitro

BMC Gastroenterology, Год журнала: 2025, Номер 25(1)

Опубликована: Фев. 5, 2025

Severe acute pancreatitis (SAP) has high morbidity, a complicated and dangerous course, many complications, including severe pulmonary complications. SAP-associated lung injury (SAP-ALI) is still significant challenge for surgeons because of its mortality. Therefore, more effective treatment methods are urgently needed. Emodin (EMO) shown tremendous potential in treating refractory diseases. However, protection mechanism SAP-ALI needs to be further clarified. This study was undertaken investigate the protective effects EMO against SAP rats alveolar epithelial cells, with particular focus on classical ferroptosis pathway. In an vivo study, forty SD were evenly split into five groups: sham operation (SO) group, biliopancreatic duct retrogradely injected 5% sodium taurocholate (STC) create + group administered via gavage following modeling, ML385 (a given inhibitor nuclear factor erythroid 2-related 2 (Nrf2)), group. vitro A549 cell lines exposed lipopolysaccharide (LPS) treated EMO. also used inhibit expression Nrf2. Pancreatic tissue damage evaluated using histological examination molecular experiments. Enzyme-linked immunosorbent assays (ELISA) assess levels pro-inflammatory cytokines, Fe2+, associated oxidative stress indicators serum supernatant. Real-time polymerase chain reaction (PCR), Western blot (WB), immunofluorescence find expressions related mRNAs proteins or cells. The findings demonstrated that suppressing Nrf2 exacerbated inflammatory response brought by pathological alterations SAP-ALI. reversed this change activating Nrf2/Heme Oxygenase-1 (HO-1)/glutathione peroxidase 4 (GPX4) signal path. Moreover, these results showed EMO, contrary ML385, suppressed response, which manifested as up-regulated glutathione (GSH) GPX4 down-regulated malondialdehyde (MDA), superoxide dismutase (SOD), reactive oxygen species (ROS) levels. Our effectively inhibited both vitro, while modulating Nrf2/HO-1/GPX4 signaling pathway provide

Язык: Английский

Pretreatment with Dexmedetomidine Protects Against Myocardial Ischemia and Reperfusion Injury Through Activation of Nrf2/Keap1/P62 Signaling

Опубликована: Янв. 1, 2024

Язык: Английский