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Gold nanoparticles reduce high glucose-induced oxidative-nitrosative stress regulated inflammation and apoptosis via tuberin-mTOR/NF-κB pathways in macrophages

Authors Rizwan H, Mohanta J, Si S, Pal A

Received 15 May 2017

Accepted for publication 27 June 2017

Published 17 August 2017 Volume 2017:12 Pages 5841—5862

DOI https://doi.org/10.2147/IJN.S141839

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Editor who approved publication: Prof. Dr. Thomas Webster


Huma Rizwan,1 Jagdeep Mohanta,2 Satyabrata Si,1,2 Arttatrana Pal3



1School of Biotechnology, KIIT University, Bhubaneswar, India; 2School of Applied Sciences, KIIT University, Bhubaneswar, India; 3Department of Zoology, School of Life Sciences, Mahatma Gandhi Central University, Bihar, India



Abstract: 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 κB (NF-κB) via ERK1/2mitogen-activated protein kinase (MAPK)/Akt/tuberin- mammalian target of rapamycin (mTOR) pathways. The activated NF-κB 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-κB by ERK1/2MAPK/Akt/tuberin-mTOR pathways-mediated inflammatory genes expression and cellular stress responses, which may be beneficial for minimizing the atherosclerosis.


Keywords: gold nanoparticles, oxidative-nitrosative stress, apoptosis, macrophages, atherosclerosis
 

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