Yong Heng Wang, Ning Li, Yi Guan, Tong Li, Yuxiu Zhang, Hong Cao, Zhi Hua Yu, Zhi Heng Li, Shuo Yan Li, Jia Hao Hu, Wen Xin Zhou, Si Si Qin, Shuang Li, San Qiao Yao
{"title":"SiO 2 在硅肺病小鼠模型中诱导心肌细胞铁超载和铁突变。","authors":"Yong Heng Wang, Ning Li, Yi Guan, Tong Li, Yuxiu Zhang, Hong Cao, Zhi Hua Yu, Zhi Heng Li, Shuo Yan Li, Jia Hao Hu, Wen Xin Zhou, Si Si Qin, Shuang Li, San Qiao Yao","doi":"10.3967/bes2024.087","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to explore the role and mechanism of ferroptosis in SiO <sub>2</sub>-induced cardiac injury using a mouse model.</p><p><strong>Methods: </strong>Male C57BL/6 mice were intratracheally instilled with SiO <sub>2</sub> 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.</p><p><strong>Results: </strong>SiO <sub>2</sub> 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 <sub>2</sub>-induced mitochondrial damage and myocardial injury. SiO <sub>2</sub> inhibited Nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant genes, while Fer-1 more potently reactivated Nrf2 compared to DFO.</p><p><strong>Conclusion: </strong>Iron overload-induced ferroptosis contributes to SiO <sub>2</sub>-induced cardiac injury. Targeting ferroptosis by reducing iron accumulation or inhibiting lipid peroxidation protects against SiO <sub>2</sub> cardiotoxicity, potentially <i>via</i> modulation of the Nrf2 pathway.</p>","PeriodicalId":93903,"journal":{"name":"Biomedical and environmental sciences : BES","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"SiO <sub>2</sub> Induces Iron Overload and Ferroptosis in Cardiomyocytes in a Silicosis Mouse Model.\",\"authors\":\"Yong Heng Wang, Ning Li, Yi Guan, Tong Li, Yuxiu Zhang, Hong Cao, Zhi Hua Yu, Zhi Heng Li, Shuo Yan Li, Jia Hao Hu, Wen Xin Zhou, Si Si Qin, Shuang Li, San Qiao Yao\",\"doi\":\"10.3967/bes2024.087\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>The aim of this study was to explore the role and mechanism of ferroptosis in SiO <sub>2</sub>-induced cardiac injury using a mouse model.</p><p><strong>Methods: </strong>Male C57BL/6 mice were intratracheally instilled with SiO <sub>2</sub> 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.</p><p><strong>Results: </strong>SiO <sub>2</sub> 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 <sub>2</sub>-induced mitochondrial damage and myocardial injury. SiO <sub>2</sub> inhibited Nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant genes, while Fer-1 more potently reactivated Nrf2 compared to DFO.</p><p><strong>Conclusion: </strong>Iron overload-induced ferroptosis contributes to SiO <sub>2</sub>-induced cardiac injury. Targeting ferroptosis by reducing iron accumulation or inhibiting lipid peroxidation protects against SiO <sub>2</sub> cardiotoxicity, potentially <i>via</i> modulation of the Nrf2 pathway.</p>\",\"PeriodicalId\":93903,\"journal\":{\"name\":\"Biomedical and environmental sciences : BES\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-06-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biomedical and environmental sciences : BES\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3967/bes2024.087\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedical and environmental sciences : BES","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3967/bes2024.087","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
SiO 2 Induces Iron Overload and Ferroptosis in Cardiomyocytes in a Silicosis Mouse Model.
Objective: The aim of this study was to explore the role and mechanism of ferroptosis in SiO 2-induced cardiac injury using a mouse model.
Methods: 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.
Results: 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.
Conclusion: 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.
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