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氮掺杂碳量子点:一种干扰淀粉样蛋白形成轨迹的多面碳纳米材料。

Nitrogen doped carbon quantum dots: a multifaceted carbon nanomaterial that interferes in an amyloid-forming trajectory.

作者信息

ElMorsy Sherin M, Gutierrez Denisse A, Valdez Salvador, Kumar Jyotish, Aguilera Renato J, Noufal Mohamed, Chinnam Sampath, Sarma Hemen, Narayan Mahesh

机构信息

The Environmental Science & Engineering Program, The University of Texas at El Paso, El Paso, TX 79968, USA.

Cellular Characterization and Biorepository Core Facility, Border Biomedical Research Center, Department of Biological Sciences, College of Science, The University of Texas at El Paso, 500 West University Avenue, El Paso, TX 79968-0519, USA.

出版信息

J Mater Chem B. 2025 Jan 22;13(4):1403-1411. doi: 10.1039/d4tb02104e.

DOI:10.1039/d4tb02104e
PMID:39670830
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11755383/
Abstract

Carbon quantum dots (CQDs) are a versatile class of carbon-based nanomaterial frameworks that have previously been used as a diagnostic device, in sensing for environmental applications, in bioimaging, and for drug delivery systems. Their versatility stems from their ability to be chemically tailored functionalization to optimize properties for specific applications. In this study, we have synthesized lactic acid-derived nitrogen doped carbon quantum dots (LAdN-CQDs) and examined their ability to intervene in the conversion of soluble, monomeric hen egg-white lysozyme (HEWL) into mature fibrils. Our data indicate that LAdN-CQDs inhibit HEWL fibril formation in a dose-dependent manner (achieving up to 50% inhibition at 2.5 mg mL). Furthermore, in a neuroblastoma-derived cell line, LAdN-CQDs were found not to disrupt mitochondrial membrane potential or trigger apoptosis at the same concentration range, suggesting that they are biocompatible. LAdN-CQDs effectively neutralized reactive oxygen species (ROS), with a 50% decrease in ROS levels at just 100 μg mL when challenged with an established free radical generator and protected the cell line from rotenone-induced apoptosis. The ability of LadN-CQDs to inhibit the soluble-to-toxic transformation of HEWL, the tolerance of SHSY-5Y cells to LAdN-CQDs, and their ability to restitute cells from rotenone-induced apoptosis, combined with the biocompatibility findings, suggest that LAdN-CQDs are potentially neuroprotective. The findings indicate that LAdN-CQDs represent a versatile, carbon-based, sustainable nanoplatform that bridges nanotechnology and neuroprotection, promoting the development of green chemistry-based healthcare solutions.

摘要

碳量子点(CQDs)是一类多功能的碳基纳米材料框架,此前已被用作诊断设备、用于环境应用传感、生物成像以及药物递送系统。它们的多功能性源于其能够通过化学定制功能化来优化特定应用的性能。在本研究中,我们合成了乳酸衍生的氮掺杂碳量子点(LAdN-CQDs),并研究了它们干预可溶性单体鸡蛋清溶菌酶(HEWL)转化为成熟纤维的能力。我们的数据表明,LAdN-CQDs以剂量依赖的方式抑制HEWL纤维形成(在2.5 mg/mL时抑制率高达50%)。此外,在一种神经母细胞瘤衍生的细胞系中,发现LAdN-CQDs在相同浓度范围内不会破坏线粒体膜电位或引发细胞凋亡,这表明它们具有生物相容性。LAdN-CQDs有效中和了活性氧(ROS),在用既定的自由基发生器攻击时,仅在100 μg/mL时ROS水平就降低了50%,并保护细胞系免受鱼藤酮诱导的细胞凋亡。LadN-CQDs抑制HEWL从可溶性向毒性转变的能力、SHSY-5Y细胞对LAdN-CQDs的耐受性,以及它们使细胞从鱼藤酮诱导的细胞凋亡中恢复的能力,再加上生物相容性研究结果,表明LAdN-CQDs具有潜在的神经保护作用。研究结果表明,LAdN-CQDs代表了一种多功能的、基于碳的、可持续的纳米平台,它架起了纳米技术与神经保护之间的桥梁,促进了基于绿色化学的医疗保健解决方案的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/ba8d9f961eab/nihms-2042923-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/6b7de4fd8d23/nihms-2042923-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/fd2a1795926c/nihms-2042923-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/3be478d3e97e/nihms-2042923-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/13325c87a4e7/nihms-2042923-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/ba8d9f961eab/nihms-2042923-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/6b7de4fd8d23/nihms-2042923-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/fd2a1795926c/nihms-2042923-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/3be478d3e97e/nihms-2042923-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/13325c87a4e7/nihms-2042923-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a283/11755383/ba8d9f961eab/nihms-2042923-f0006.jpg

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Rotenone Induces a Neuropathological Phenotype in Cholinergic-like Neurons Resembling Parkinson's Disease Dementia (PDD).
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