Department of Nutrition and Food Hygiene, School of Public Health, Hebei Key Laboratory of Environment and Human Health, Hebei Medical University, Shijiazhuang, 050017, China.
Undergraduate of College of Public Health, Hebei Medical University, Shijiazhuang, 050017, China.
Cell Mol Biol Lett. 2023 Nov 25;28(1):95. doi: 10.1186/s11658-023-00513-1.
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)-induced cardiomyocyte damage and its underlying mechanisms remain unclear.
In vitro experiments, the H9C2 cells were subjected to pretreatment with varying concentrations of AST, and then cardiomyocyte injury model induced by PM 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 injury was established by intratracheal instillation every other day for 1 week. The effects of AST on myocardial tissue injury caused by PM indicating by histological, serum, and protein analyses were examined.
AST significantly ameliorated PM-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.
Our study suggest that ferroptosis plays a significant role in the pathogenesis of cardiomyocyte injury induced by PM. AST may serve as a potential therapeutic agent for mitigating cardiomyocyte injury caused by PM through the inhibition of ferroptosis.
人类长期暴露于空气污染与心血管疾病（CVD）风险增加有关。虾青素（AST）是一种天然存在的红色类胡萝卜素色素，已被证明具有多种健康益处。然而，AST 是否对细颗粒物（PM）诱导的心肌细胞损伤具有保护作用及其潜在机制尚不清楚。
在体外实验中，用不同浓度的 AST 预处理 H9C2 细胞，然后建立 PM 诱导的心肌细胞损伤模型。在不同组中测量细胞活力和铁死亡相关蛋白的表达。在体内实验中，用不同浓度的 AST 预处理大鼠 21 天。然后，通过气管内滴注每天间隔 1 次，持续 1 周，建立大鼠 PM 心肌损伤模型。通过组织学、血清和蛋白质分析检测 AST 对 PM 引起的心肌组织损伤的影响。
AST 显著改善了 PM 诱导的心肌组织损伤、炎症细胞浸润、炎症因子释放和心肌细胞 H9C2 损伤。机制上，AST 预处理可增加体外和体内 SLC7A11、GPX4 的表达，降低 TfR1、FTL 和 FTH1 的表达。
我们的研究表明，铁死亡在 PM 诱导的心肌细胞损伤发病机制中起重要作用。AST 可能通过抑制铁死亡成为减轻 PM 引起的心肌细胞损伤的潜在治疗剂。
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