Oncotarget

Research Papers:

Inhibition of nuclear factor-κB signal by pyrrolidine dithiocarbamate alleviates lipopolysaccharide-induced acute lung injury

Hongfu Yang _, Rongqing Sun, Ning Ma, Qilong Liu, Xiaoge Sun, Panpan Zi, Junsheng Wang, Ke Chao and Lei Yu

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Oncotarget. 2017; 8:47296-47304. https://doi.org/10.18632/oncotarget.17624

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Abstract

Hongfu Yang1, Rongqing Sun1, Ning Ma1, Qilong Liu1, Xiaoge Sun1, Panpan Zi1, Junsheng Wang1, Ke Chao1 and Lei Yu1

1Critical Care Medical Department, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450000, P.R. China

Correspondence to:

Hongfu Yang, email: yanghongfu_y@yeah.net

Keywords: NF-κB, acute lung injury, inflammation, oxidative stress, mitochondrial function

Received: January 20, 2017     Accepted: April 11, 2017     Published: May 04, 2017

ABSTRACT

This study mainly studied the effect of inhibition of nuclear factor-κB (NF-κB) signal by pyrrolidine dithiocarbamate (PDTC) on lipopolysaccharide (LPS)-induced inflammatory response, oxidative stress, and mitochondrial dysfunction in a murine acute lung injury model. The results showed that LPS exposure activated NF-κB and its upstream proteins and caused lung inflammation, oxidative stress, and mitochondrial dysfunction in mice. While inhibition of NF-κB by PDTC adminstration alleviated LPS-induced generation of lymphocytes, IL-1β, and TNF-α. Malondialdehyde, a common oxidative product, was markedly reduced after PDTC treatment in LPS-challenged mice. Furthermore, PDTC alleviated LPS-induced mitochondrial dysfunction via improving ATP synthesis and uncoupling protein 2 expression. In conclusion, inhibition of NF-κB by PDTC alleviated LPS-induced acute lung injury via maintaining inflammatory status, oxidative balance, and mitochondrial function in mice.


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