金纳米颗粒-氧化铁颗粒赋予骨支架抗肿瘤功能。

IF 3.6 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-02-18 DOI:10.1080/10715762.2025.2466246
Tiantian He, Wenjing Yang, Youwen Yang, Shuping Peng, Cijun Shuai
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引用次数: 0

摘要

氧化铁(Fe-O)具有抗肿瘤的特性,因为它能够催化肿瘤细胞的过氧化氢(H2O2)产生活性氧(ROS),从而引起铁下垂。由于肿瘤细胞中H2O2不足,其抗肿瘤性能受到限制。一种纳米药物,金纳米颗粒(NPs)生长在Fe-O上,整合到聚l -丙交酯(PLLA)支架中。结果表明,Au NPs可以消耗肿瘤细胞的葡萄糖产生H2O2,补充反应底物。PLLA/Au@Fe-O支架对MG63表现出增强的抗肿瘤活性,包括增加死亡率、减少迁移和菌落形成。PLLA/Au@Fe-O支架促进MG63铁下垂,包括上调COX-2蛋白,下调FTH1蛋白和GPX4蛋白。PLLA/Au@Fe-O支架也促进MG63的自噬,包括下调P62蛋白,上调LC3BII/I。从机制上讲,PLLA/Au@Fe-O支架通过促进铁下垂和自噬来增强抗肿瘤活性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Gold nanoparticles-supported iron oxide particles endows bone scaffolds with anti-tumor function.

Iron oxide (Fe-O) has anti-tumor properties, due to its ability of catalyzing hydrogen peroxide (H2O2) of tumor cells to generate reactive oxygen species (ROS) and then cause ferroptosis. Its anti-tumor performance is restricted due to insufficient H2O2 in tumor cells. A nanomedicine, Au nanoparticles (NPs) grown on Fe-O, was integrated into poly-l-lactide (PLLA) scaffolds. Results indicated that Au NPs could consume glucose of tumor cells to produce H2O2, which supplemented reaction substrate. PLLA/Au@Fe-O scaffold showed enhanced anti-tumor activities against MG63, including increased mortality, decreased migration and colony formation. PLLA/Au@Fe-O scaffold promoted ferroptosis in MG63, including up-regulation of COX-2 protein, down-regulation of FTH1 protein and GPX4 protein. PLLA/Au@Fe-O scaffold also promoted autophagy in MG63, including down-regulation of P62 protein, and up-regulation of LC3BII/I. Mechanistically, PLLA/Au@Fe-O scaffold possessed enhanced anti-tumor activities through promoting ferroptosis and autophagy.

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来源期刊
Free Radical Research
Free Radical Research 生物-生化与分子生物学
CiteScore
6.70
自引率
0.00%
发文量
47
审稿时长
3 months
期刊介绍: Free Radical Research publishes high-quality research papers, hypotheses and reviews in free radicals and other reactive species in biological, clinical, environmental and other systems; redox signalling; antioxidants, including diet-derived antioxidants and other relevant aspects of human nutrition; and oxidative damage, mechanisms and measurement.
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