期刊
INTERNATIONAL JOURNAL OF NANOMEDICINE
卷 12, 期 -, 页码 5841-5862出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/IJN.S141839
关键词
gold nanoparticles; oxidative-nitrosative stress; apoptosis; macrophages; atherosclerosis
资金
- Department of Biotechnology, government of India [BT/PR14241/MED/30/423/2010]
- Department of Sciences and Technology, government of India [SB/FT/CS/-096/2012]
- University Grant Commission-Maulana Azad National Fellowship
Hyperglycemia is a risk factor for cardiovascular mortality and morbidity, and directly responsible for exacerbating macrophage activation and atherosclerosis. We showed that gold nanoparticles (AuNPs) reduce the high glucose (HG)-induced atherosclerosis-related complications in macrophages via oxidative-nitrosative stress-regulated inflammation and apoptosis. The effects of AuNPs on oxidative-nitrosative stress markers such as cellular antioxidants were attenuated by HG exposure, leading to reduction in the accumulation of reactive oxygen/nitrogen species in cellular compartments. Further, these abnormalities of antioxidants level and reactive oxygen/nitrogen species accumulations initiate cellular stress, resulting in the activation of nuclear factor kappa B (NF-kappa B) via ERK1/2mitogen-activated protein kinase (MAPK)/Akt/tuberin-mammalian target of rapamycin (mTOR) pathways. The activated NF-kappa B stimulates inflammatory mediators, which subsequently subdue biomolecules damage, leading to aggravation of the inflammatory infiltration and immune responses. Treatment of AuNPs inhibits the intracellular redox-sensitive signaling pathways, inflammation, and apoptosis in macrophages. Together, our results indicate that AuNPs may modulate HG-induced oxidative-nitrosative stress. These effects may be sealed tight due to the fact that AuNPs treatment reduces the activation of NF-kappa B by ERK1/2MAPK/Akt/tuberin-mTOR pathways-mediated inflammatory genes expression and cellular stress responses, which may be beneficial for minimizing the atherosclerosis.
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