Nrf2 protects against oxidative stress induced by SiO2 nanoparticles

Aim: The aim of our study was to explore the role of nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) on the exposure of SiO2 nanoparticles (NPs) and its influence. Materials & methods: To understand the mechanism of NP-induced oxidative stress, the involvement of oxidative-stress-resp...

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Bibliographic Details
Published in:Nanomedicine (London, England) England), 2017-10, Vol.12 (19), p.2303
Main Authors: Liu, Wei, Hu, Tao, Zhou, Li, Wu, Desheng, Huang, Xinfeng, Ren, Xiaohu, Lv, Yuan, Hong, Wenxu, Huang, Guanqin, Lin, Zequn, Liu, Jianjun
Format: Article
Language:English
Subjects:
Antioxidants
Cancer
Cell cycle
Cytotoxicity
Endoplasmic reticulum
Inflammation
Inflammatory bowel disease
Kinases
Nanoparticles
Oxidative stress
Proteins
Reactive oxygen species
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Summary:Aim: The aim of our study was to explore the role of nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) on the exposure of SiO2 nanoparticles (NPs) and its influence. Materials & methods: To understand the mechanism of NP-induced oxidative stress, the involvement of oxidative-stress-responding transcription factors and the Nrf2/antioxidant reactive element (ARE) signaling pathway in the toxicity of SiO2 NPs’ exposure was investigated via in vivo and in vitro models. Results: A549 cells showed a significant cytotoxic effect while A549-shNrf2 cells showed decreased cell viability after nm-SiO2 exposure. SiO2 NPs’ exposure activated the Nrf2/ARE signaling pathway. Nrf2−/− exposed mice showed increased reactive oxygen species, 8-hydroxyl deoxyguanosine level and decreased total antioxidant capacity. Nrf2/ARE signaling pathway activation disrupted, leading inhibition of heme oxygenase-1 and upregulation of PKR-like endoplasmic-reticulum-regulated kinase. Conclusion: Our findings suggested that Nrf2 could protect against oxidative stress induced by SiO2 NPs, and the Nrf2/ARE pathway might be involved in mild-to-moderate SiO2 NP-induced oxidative stress that was evident from dampened activity of Nrf2.
ISSN:1743-5889
1748-6963
DOI:10.2217/nnm-2017-0046