Astaxanthin alleviates PM2.5-induced cardiomyocyte injury via inhibiting ferroptosis

作者：Jingyi Ren, Bowen Yin, Zihao Guo, Xiaoya Sun, Huanting Pei, Wen Rui, Ziyi Wang, Siqi Zhu, Jinshi Zuo, Yadong Zhang, Yuxia Ma · 发表于：Cellular & Molecular Biology Letters · 年份：2023 · DOI：10.1186/s11658-023-00513-1 · 被引用次数：34 · 研究领域：Air Quality and Health Impacts、Ferroptosis and cancer prognosis、Biomarkers in Disease Mechanisms

Abstract Background Long-term exposure of humans to air pollution is associated with an increasing risk of cardiovascular diseases (CVDs). Astaxanthin (AST), a naturally occurring red carotenoid pigment, was proved to have multiple health benefits. However, whether or not AST also exerts a protective effect on fine particulate matter (PM 2.5 )-induced cardiomyocyte damage and its underlying mechanisms remain unclear. Methods In vitro experiments, the H9C2 cells were subjected to pretreatment with varying concentrations of AST, and then cardiomyocyte injury model induced by PM 2.5 was established. The cell viability and the ferroptosis-related proteins expression were measured in different groups. In vivo experiments, the rats were pretreated with different concentrations of AST for 21 days. Subsequently, a rat model of myocardial PM 2.5 injury was established by intratracheal instillation every other day for 1 week. The effects of AST on myocardial tissue injury caused by PM 2.5 indicating by histological, serum, and protein analyses were examined. Results AST significantly ameliorated PM 2.5 -induced myocardial tissue injury, inflammatory cell infiltration, the release of inflammatory factors, and cardiomyocyte H9C2 cell damage. Mechanistically, AST pretreatment increased the expression of SLC7A11, GPX4 and down-regulated the expression of TfR1, FTL and FTH1 in vitro and in vivo. Conclusions Our study suggest that ferroptosis plays a significant role in the pathogenesis of c...