Abstract：
UNASSIGNED: The aim of this study was to explore the role and mechanism of ferroptosis in SiO 2-induced cardiac injury using a mouse model.
UNASSIGNED: Male C57BL/6 mice were intratracheally instilled with SiO 2 to create a silicosis model. Ferrostatin-1 (Fer-1) and deferoxamine (DFO) were used to suppress ferroptosis. Serum biomarkers, oxidative stress markers, histopathology, iron content, and the expression of ferroptosis-related proteins were assessed.
UNASSIGNED: SiO 2 altered serum cardiac injury biomarkers, oxidative stress, iron accumulation, and ferroptosis markers in myocardial tissue. Fer-1 and DFO reduced lipid peroxidation and iron overload, and alleviated SiO 2-induced mitochondrial damage and myocardial injury. SiO 2 inhibited Nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant genes, while Fer-1 more potently reactivated Nrf2 compared to DFO.
UNASSIGNED: Iron overload-induced ferroptosis contributes to SiO 2-induced cardiac injury. Targeting ferroptosis by reducing iron accumulation or inhibiting lipid peroxidation protects against SiO 2 cardiotoxicity, potentially via modulation of the Nrf2 pathway.
UNASSIGNED: Male C57BL/6 mice were intratracheally instilled with SiO 2 to create a silicosis model. Ferrostatin-1 (Fer-1) and deferoxamine (DFO) were used to suppress ferroptosis. Serum biomarkers, oxidative stress markers, histopathology, iron content, and the expression of ferroptosis-related proteins were assessed.
UNASSIGNED: SiO 2 altered serum cardiac injury biomarkers, oxidative stress, iron accumulation, and ferroptosis markers in myocardial tissue. Fer-1 and DFO reduced lipid peroxidation and iron overload, and alleviated SiO 2-induced mitochondrial damage and myocardial injury. SiO 2 inhibited Nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant genes, while Fer-1 more potently reactivated Nrf2 compared to DFO.
UNASSIGNED: Iron overload-induced ferroptosis contributes to SiO 2-induced cardiac injury. Targeting ferroptosis by reducing iron accumulation or inhibiting lipid peroxidation protects against SiO 2 cardiotoxicity, potentially via modulation of the Nrf2 pathway.
摘要：
■这项研究的目的是使用小鼠模型探索铁凋亡在SiO2诱导的心脏损伤中的作用和机制。
■雄性C57BL/6小鼠气管内滴注SiO2以创建矽肺模型。使用Ferrostatin-1（Fer-1）和去铁胺（DFO）来抑制铁凋亡。血清生物标志物，氧化应激标志物，组织病理学,铁含量,并评估铁凋亡相关蛋白的表达。
■SiO2改变了血清心脏损伤生物标志物，氧化应激，铁积累，和心肌组织中的铁性凋亡标志物。Fer-1和DFO减少脂质过氧化和铁过载，减轻SiO2诱导的线粒体损伤和心肌损伤。SiO2抑制核因子类2相关因子2（Nrf2）及其下游抗氧化基因，与DFO相比，Fer-1更有效地重新激活Nrf2。
■铁过载诱导的铁凋亡有助于SiO2诱导的心脏损伤。通过减少铁积累或抑制脂质过氧化来靶向铁凋亡，可以防止SiO2心脏毒性，可能通过Nrf2途径的调节。
■雄性C57BL/6小鼠气管内滴注SiO2以创建矽肺模型。使用Ferrostatin-1（Fer-1）和去铁胺（DFO）来抑制铁凋亡。血清生物标志物，氧化应激标志物，组织病理学,铁含量,并评估铁凋亡相关蛋白的表达。
■SiO2改变了血清心脏损伤生物标志物，氧化应激，铁积累，和心肌组织中的铁性凋亡标志物。Fer-1和DFO减少脂质过氧化和铁过载，减轻SiO2诱导的线粒体损伤和心肌损伤。SiO2抑制核因子类2相关因子2（Nrf2）及其下游抗氧化基因，与DFO相比，Fer-1更有效地重新激活Nrf2。
■铁过载诱导的铁凋亡有助于SiO2诱导的心脏损伤。通过减少铁积累或抑制脂质过氧化来靶向铁凋亡，可以防止SiO2心脏毒性，可能通过Nrf2途径的调节。
