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姜黄素-聚多巴胺纳米颗粒通过铁螯合和抑制氧化应激损伤减轻铁死亡。

Curcumin-polydopamine nanoparticles alleviate ferroptosis by iron chelation and inhibition of oxidative stress damage.

作者信息

Lei Li, Yuan Jiali, Yang Qingqing, Tu Qiuxia, Yu Haijun, Chu Liangzhao, Tang Lei, Zhang Chunlin

机构信息

Engineering Research Center for Molecular Medicine, School of Basic Medical Science, Guizhou Medical University Guiyang 550025 China.

Department of Neurosurgery, The Affiliated Hospital of Guizhou Medical University Guiyang Guizhou China.

出版信息

RSC Adv. 2024 May 7;14(21):14934-14941. doi: 10.1039/d4ra02336f. eCollection 2024 May 2.

DOI:10.1039/d4ra02336f
PMID:38716098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11075776/
Abstract

Ferroptosis, characterized by elevated iron levels and lipid peroxidation (LPO), is a recently identified regulatory mechanism of cell death. Its substantial involvement in ischemic tissue injury, neurodegenerative disorders, and cancer positions ferroptosis inhibition as a promising strategy for managing these diverse diseases. In this study, we introduce curcumin-polydopamine nanoparticles (Cur-PDA NPs) as an innovative ferroptosis inhibitor. Cur-PDA NPs demonstrate remarkable efficacy in chelating both Fe and Fe along with scavenging free radicals. Cur-PDA NPs were found to efficiently mitigate reactive oxygen species, reduce Fe accumulation, suppress LPO, and rejuvenate mitochondrial function in PC12 cells. Thus, these NPs can act as potent therapeutic agents against ferroptosis, primarily iron chelation and reduction of oxidative stress.

摘要

铁死亡以铁水平升高和脂质过氧化(LPO)为特征,是最近发现的一种细胞死亡调节机制。它在缺血性组织损伤、神经退行性疾病和癌症中大量参与,使得抑制铁死亡成为治疗这些多种疾病的一种有前景的策略。在本研究中,我们引入姜黄素-聚多巴胺纳米颗粒(Cur-PDA NPs)作为一种创新的铁死亡抑制剂。Cur-PDA NPs在螯合Fe和Fe以及清除自由基方面表现出显著功效。研究发现Cur-PDA NPs能有效减轻活性氧,减少铁积累,抑制LPO,并恢复PC12细胞的线粒体功能。因此,这些纳米颗粒可作为对抗铁死亡的有效治疗剂,主要通过铁螯合和降低氧化应激来实现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50b/11075776/9b00377e8a28/d4ra02336f-f6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50b/11075776/89d806179bc4/d4ra02336f-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50b/11075776/10f02ed02bf2/d4ra02336f-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50b/11075776/9b00377e8a28/d4ra02336f-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50b/11075776/a1fbad1314a4/d4ra02336f-s1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50b/11075776/e3e1f102e005/d4ra02336f-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50b/11075776/f1285a989a75/d4ra02336f-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50b/11075776/fba7018a27cf/d4ra02336f-f3.jpg
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Gen Psychiatr. 2023 Oct 19;36(5):e101072. doi: 10.1136/gpsych-2023-101072. eCollection 2023.
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Emerging significance and therapeutic targets of ferroptosis: a potential avenue for human kidney diseases.铁死亡的新意义和治疗靶点:人类肾脏病的一个潜在途径。
Cell Death Dis. 2023 Sep 22;14(9):628. doi: 10.1038/s41419-023-06144-w.
3
Mesenchymal stem cell attenuates spinal cord injury by inhibiting mitochondrial quality control-associated neuronal ferroptosis.
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Redox Biol. 2023 Nov;67:102871. doi: 10.1016/j.redox.2023.102871. Epub 2023 Sep 7.
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Research on ferroptosis as a therapeutic target for the treatment of neurodegenerative diseases.将铁死亡作为神经退行性疾病治疗靶点的研究。
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The diversified role of mitochondria in ferroptosis in cancer.线粒体在癌症中铁死亡中的多样化作用。
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