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首页> 外文期刊>Nanoscale Research Letters >Gold Nanoparticles of Diameter 13?nm Induce Apoptosis in Rabbit Articular Chondrocytes
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Gold Nanoparticles of Diameter 13?nm Induce Apoptosis in Rabbit Articular Chondrocytes

机译:直径13?nm的金纳米颗粒诱导兔关节软骨细胞凋亡。

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Gold nanoparticles (AuNPs) have been widely used in biomedical science including antiarthritic agents, drug loading, and photothermal therapy. In this report, we studied the effects of AuNPs with diameters of 3, 13, and 45?nm, respectively, on rabbit articular chondrocytes. AuNPs were capped with citrate and their diameter and zeta potential were measured by dynamic light scattering (DLS). Cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay after the rabbit articular chondrocytes were pre-incubated with 3, 13, and 45?nm AuNPs, respectively, for 24?h. Flow cytometry (FCM) analysis with annexin V/propidium iodide (PI) double staining and fluorescence imaging with Hoechst 33258 staining were used to determine the fashion of AuNPs-induced chondrocyte death. Further, 13?nm AuNPs (2 nM) significantly induced chondrocyte death accompanying apoptotic characteristics including mitochondrial damage, externalization of phosphatidylserine and nuclear concentration. However, 3?nm AuNPs (2 nM) and 45?nm (0.02 nM) AuNPs did not induce cytotoxicity in chondrocytes. Although 13?nm AuNPs (2 nM) increased the intracellular reactive oxygen species (ROS) level, pretreatment with Nacetyl cysteine (NAC), a ROS scavenger, did not prevent the cytotoxicity induced by 13?nm AuNPs, indicating that 13?nm AuNPs (2 nM) induced ROS-independent apoptosis in chondrocytes. These results demonstrate the size-dependent cytotoxicity of AuNPs in chondrocytes, which must be seriously considered when using AuNPs for treatment of osteoarthritis (OA).
机译:金纳米颗粒(AuNPs)已广泛用于生物医学科学,包括抗关节炎药,载药量和光热疗法。在本报告中,我们研究了直径分别为3、13和45?nm的AuNP对兔关节软骨细胞的影响。 AuNPs用柠檬酸盐封盖,并通过动态光散射(DLS)测量其直径和Zeta电位。在分别将兔关节软骨细胞分别与3、13和45nm nm AuNPs孵育24?h之后,通过Cell Counting Kit-8(CCK-8)分析评估细胞活力。流式细胞术(FCM)分析与膜联蛋白V /碘化丙啶(PI)双重染色和Hoechst 33258染色的荧光成像被用来确定AuNPs诱导软骨细胞死亡的方式。此外,13nm的AuNPs(2 nM)显着诱导软骨细胞死亡,并伴有凋亡特征,包括线粒体损伤,磷脂酰丝氨酸的外在化和核浓度。但是,3?nm AuNPs(2 nM)和45?nm(0.02 nM)AuNPs不会诱导软骨细胞的细胞毒性。尽管13?nm AuNPs(2 nM)增加了细胞内活性氧(ROS)的水平,但用ROS清道夫N乙酰半胱氨酸(NAC)预处理并不能阻止13?nm AuNPs诱导的细胞毒性,表明13?nm AuNPs (2 nM)诱导软骨细胞中非ROS依赖性凋亡。这些结果证明了软骨细胞中AuNPs的大小依赖性细胞毒性,在使用AuNPs治疗骨关节炎(OA)时必须认真考虑。

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