LLDPE/TiO2-ZnO纳米复合膜诱导人成纤维细胞和血细胞模型的瞬态氧化应激反应

IF 0.5 Q4 ENGINEERING, BIOMEDICAL
Nor Hazliana Harun, R. Mydin, S. Sreekantan, Khairul Arifah Saharuddin, A. Seeni
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引用次数: 0

摘要

医疗保健相关感染(HAI)是全球主要的安全问题,会导致患者死亡率,尤其是与留置或植入医疗设备相关的患者。嵌入聚合物基体中的先进金属氧化物纳米复合材料(MNPs)具有出色的抗菌性能,特别是由于活性氧(ROS)和自由基的作用模式,对MDR菌株具有显著的抗菌性能。到目前为止,仍然缺乏关于基于MNPs的聚合物的外部反应物种对人类的影响的知识。本研究在分子基因和蛋白质水平上研究了嵌入线性低密度聚乙烯(LLDPE/TiO2-ZnO)中的TiO2-Zn纳米复合膜对人成纤维细胞和血细胞系模型的生物相互作用。对成纤维细胞和血细胞系模型的体外生物相互作用反应的初步分析显示,细胞膜完整性紊乱的迹象,这可能是由于自由基的活性,例如在TiO2–ZnO聚合物纳米复合膜的初始细胞适应过程中,细胞内ROS和Zn离子(Zn2+)的释放。进一步的研究发现,细胞-聚合物纳米复合膜的相互作用可能通过NF-kβ相互作用触发短暂的氧化应激反应和细胞氧化还原调节。然而,还需要进一步的综合研究来支持这项研究,尤其是涉及动物模型的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LLDPE/TiO2-ZnO Nanocomposite Films induces Transitory Oxidative Stress Response on Human Fibroblast and Blood Cell Lines Models
Healthcare-associated infections (HAIs) are a major safety concern globally that contribute to mortality rates amongst patients especially associated with indwelling or implanted medical devices. The advanced metal-oxide nanocomposites (MNPs) embedded in polymer matrix present an outstanding antibacterial profile, especially for MDR strains owing to reactive oxygen species (ROS) and free radicals’ mode of action. To date, there is still a lack of knowledge on the implication of external reactive species from MNPs-based polymers to humans. This study investigates the bio-interaction of TiO2-ZnO nanocomposite films embedded in linear low-density polyethylene (LLDPE/ TiO2-ZnO) on human fibroblast and blood cell lines model at molecular genes and protein level. The initial analysis of the in vitro bio-interaction responses on fibroblast and blood cell line models showed signs of cell membrane integrity disturbance, which might be due to free radicals’ activities, such as the release of intracellular ROS and Zn ions (Zn2+) during the initial cellular adaptation process on the TiO2–ZnO polymer nanocomposite film. Further findings found that cell–polymer nanocomposite film interaction could possibly trigger transitory oxidative stress response and cellular redox regulation via NF-kβ interactions. However, further comprehensive studies are needed to support this study, especially involving animal models.
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CiteScore
1.40
自引率
14.30%
发文量
73
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