Zhao Peipei, Chen Xiaojing, Wang Qiaoling, Zou Hanbing, Xie Yuexia, Liu Hongmei, Zhou Yan, Liu Peifeng, Dai Huili
Department of Nephrology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, PR China.
State Key Laboratory of Oncogenes & Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200032, PR China.
Nanomedicine (Lond). 2020 May;15(11):1079-1096. doi: 10.2217/nnm-2019-0417. Epub 2020 Feb 7.
To research the influence and mechanism of gold nanoparticles (AuNPs) with different size for HK-2 cells (kidney normal cells) and 786-0 cells (kidney cancer cells). HK-2 cells and 786-0 cells were treated with 5 and 200 nm AuNPs at 1 and 10 μg/ml. The cell viability, intracellular reactive oxygen species levels, cell apoptosis, cell autophagy, and related cell signaling pathways were analyzed. In HK-2 cells, AuNPs reduced the activity of Akt and mTOR and upregulated the expression of LC3 II. In 786-0 cells, the activity of p38 was upregulated, which leaded to the increase of caspase 3 and initiated apoptosis. AuNPs of 5 and 200 nm at 10 μg/ml exerted antitumor effect by prompting apoptosis and inhibiting proliferation, while autophagy was activated to protect HK-2 cells from AuNPs-induced cytotoxicity.
研究不同尺寸的金纳米颗粒(AuNPs)对HK-2细胞(肾正常细胞)和786-0细胞(肾癌细胞)的影响及其机制。将HK-2细胞和786-0细胞分别用浓度为1和10μg/ml的5和200nm AuNPs处理。分析细胞活力、细胞内活性氧水平、细胞凋亡、细胞自噬及相关细胞信号通路。在HK-2细胞中,AuNPs降低了Akt和mTOR的活性并上调了LC3 II的表达。在786-0细胞中,p38的活性上调,导致caspase 3增加并引发凋亡。浓度为10μg/ml的5和200nm AuNPs通过促进凋亡和抑制增殖发挥抗肿瘤作用,同时激活自噬以保护HK-2细胞免受AuNPs诱导的细胞毒性。