Inhibition of nuclear factor-?B signal by pyrrolidine dithiocarbamate alleviates lipopolysaccharide-induced acute lung injury.

ABSTRACT: This study mainly studied the effect of inhibition of nuclear factor-?B (NF-?B) 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-?B and its upstream proteins and caused lung inflammation, oxidative stress, and mitochondrial dysfunction in mice. While inhibition of NF-?B by PDTC adminstration alleviated LPS-induced generation of lymphocytes, IL-1?, and TNF-?. 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-?B by PDTC alleviated LPS-induced acute lung injury via maintaining inflammatory status, oxidative balance, and mitochondrial function in mice.

SUBMITTER: Yang H 

PROVIDER: S-EPMC5564565 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature