Targeting Ferroptosis by Polydopamine Nanoparticles Protects Heart against Ischemia/Reperfusion Injury
Targeting Ferroptosis by Polydopamine Nanoparticles Protects Heart against Ischemia/Reperfusion Injury
复制标题
聚多巴胺纳米颗粒靶向铁死亡可保护心脏免受缺血/再灌注损伤
DOI：
10.1021/acsami.1c18061
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发表时间：
2021
影响因子：
9.5
通讯作者：
Li Qian
中科院分区：
文献类型：
--
作者：
Zhang Yabing;Ren Xiangyi;Wang Yan;Chen Dongxu;Jiang Ling;Li Xi;Li Tao;Huo Minfeng;Li Qian
铁凋亡是一种新的调节性细胞死亡形式，取决于铁（Fe 2+）和脂质过氧化水平升高。心肌缺血/再灌注（I/R）损伤与铁凋亡密切相关。因此，抗铁凋亡药物被认为是治疗心肌I/R损伤的新策略。在这里，我们开发了聚多巴胺纳米颗粒（PDA NPs）作为一种新型的铁凋亡抑制剂的心脏保护。PDA NPs在抑制H9 c2细胞中Fe 2+积累和恢复线粒体功能方面具有有趣的特性。随后，我们证明了PDA纳米颗粒的管理有效地减少了Fe 2+沉积和脂质过氧化作用在心肌I/R损伤小鼠模型。此外，PDA NPs治疗减轻了小鼠心肌I/R损伤，如通过减少梗死面积和改善心脏功能所证明的。目前的工作表明PDA纳米颗粒通过防止铁凋亡对心肌I/R损伤的治疗作用。
Ferroptosis is a new form of regulated cell death depending on elevated iron (Fe2+) and lipid peroxidation levels. Myocardial ischemia/reperfusion (I/R) injury has been shown to be closely associated with ferroptosis. Therefore, antiferroptosis agents are considered to be a new strategy for managing myocardial I/R injury. Here, we developed polydopamine nanoparticles (PDA NPs) as a new type of ferroptosis inhibitor for cardioprotection. The PDA NPs features intriguing properties in inhibiting Fe2+accumulation and restoring mitochondrial functions in H9c2 cells. Subsequently, we demonstrated that administration of PDA NPs effectively reduced Fe2+deposition and lipid peroxidation in a myocardial I/R injury mouse model. In addition, the myocardial I/R injury in mice was alleviated by PDA NPs treatment, as demonstrated by reduced infarct size and improved cardiac functions. The present work indicates the therapeutic effects of PDA NPs against myocardial I/R injury via preventing ferroptosis.