Anti-Inflammatory Effect and Cellular Uptake Mechanism of Carbon Nanodots in in Human Microvascular Endothelial Cells.
Anti-Inflammatory Effect and Cellular Uptake Mechanism of Carbon Nanodots in in Human Microvascular Endothelial Cells.
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纳米碳点对人微血管内皮细胞的抗炎作用及细胞摄取机制。
DOI：
10.3390/nano11051247
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发表时间：
2021-05-10
期刊：
影响因子：
--
通讯作者：
Jia Z
中科院分区：
文献类型：
--
作者：
Belperain S;Kang ZY;Dunphy A;Priebe B;Chiu NHL;Jia Z
由于心血管疾病（CVD）引起的死亡率稳步上升，该疾病已成为医学研究领域中日益重要的主题。随着纳米技术的最新进展，已经开始推动利用这些新材料的新的CVD治疗方法。碳纳米点（CarbonNanodots，CND）是一种新型的纳米粒子，由于其绿色合成方法、生物相容性、荧光性能和潜在的抗氧化性能而备受关注。随着大量的研究涌入CND被用作生物成像和药物递送工具，很少有研究已经完成其抗炎潜力，特别是在心血管系统。CVD最初由内皮细胞炎症开始。这种炎症的原因可能来自许多来源;其中之一是肿瘤坏死因子（TNF-α），它不仅可以引发炎症，还可以通过引起促炎细胞因子的风暴来延长其存在。本研究探讨了CND减轻TNF-α诱导的人微血管内皮细胞（HMEC-1）炎症的能力。结果表明，非细胞毒性浓度的CND降低促炎基因的表达，主要是白细胞介素-8（IL-8）和白细胞介素1 β（IL-1β）。检测HMEC-1 s对CND的摄取。涉及通道阻滞剂和内吞作用干扰剂的研究结果表明，摄取通过内吞作用发生。这些发现为研究CND与经历TNF-α诱导的细胞炎症的内皮细胞的相互作用提供了新的见解。
Cardiovascular disease (CVD) has become an increasingly important topic in the field of medical research due to the steadily increasing rates of mortality caused by this disease. With recent advancements in nanotechnology, a push for new, novel treatments for CVD utilizing these new materials has begun. Carbon Nanodots (CNDs), are a new form of nanoparticles that have been coveted due to the green synthesis method, biocompatibility, fluorescent capabilities and potential anti-antioxidant properties. With much research pouring into CNDs being used as bioimaging and drug delivery tools, few studies have been completed on their anti-inflammatory potential, especially in the cardiovascular system. CVD begins initially by endothelial cell inflammation. The cause of this inflammation can come from many sources; one being tumor necrosis factor (TNF-α), which can not only trigger inflammation but prolong its existence by causing a storm of pro-inflammatory cytokines. This study investigated the ability of CNDs to attenuate TNF-α induced inflammation in human microvascular endothelial cells (HMEC-1). Results show that CNDs at non-cytotoxic concentrations reduce the expression of pro-inflammatory genes, mainly Interleukin-8 (IL-8), and interleukin 1 beta (IL-1β). The uptake of CNDs by HMEC-1s was examined. Results from the studies involving channel blockers and endocytosis disruptors suggest that uptake takes place by endocytosis. These findings provide insights on the interaction CNDs and endothelial cells undergoing TNF-α induced cellular inflammation.
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影响因子：
46.2
作者：
Behzadi S;Serpooshan V;Tao W;Hamaly MA;Alkawareek MY;Dreaden EC;Brown D;Alkilany AM;Farokhzad OC;Mahmoudi M
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16
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影响因子：
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作者：
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通讯作者：
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