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Title 

Thioredoxin-interacting protein-derived peptide (TN13) inhibits LPS-induced inflammation by inhibiting p38 MAPK signaling

Authors 

Dong Oh KimJae-Eun ByunH A SeongSuk Ran YoonInoyo ChoiHaiyoung Jung

Publisher 

Elsevier

Issue Date 

2018

Citation 

Biochemical and Biophysical Research Communications

Keywords 

InflammationLPSMacrophageTN13TXNIPp38 MAPK

Abstract 

Inflammation comprises an innate immune response, and is mainly induced by macrophages to protect the host from pathogens and mechanical injuries. The p38 mitogen-activated protein kinase (MAPK) pathway is a key regulator of inflammatory responses in macrophages. Here, we investigated the anti-inflammatory effects of thioredoxin-interacting protein-derived peptide (TN13) in macrophages in vitro and in vivo. Human immunodeficiency virus (HIV) trans-activator protein (TAT)-conjugated TN13 (TAT-TN13) was found to penetrate RAW 264.7?cells and decrease p38 MAPK activation in a dose-dependent manner. We also showed that TAT-TN13 could significantly inhibit lipopolysaccharide (LPS)-induced expression of macrophage activation-related receptors including CD80, CD86, and MHC II, as well as the transcriptional activation of nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1) in RAW 264.7?cells and primary mouse splenic macrophages. Furthermore, TAT-TN13 decreased the LPS-induced production of proinflammatory cytokines and mediators such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), nitric oxide (NO), inducible NO synthase (iNOS), and cyclooxygenase 2 (COX-2) in RAW 264.7?cells and mice. These results indicate that TAT-TN13 can inhibit macrophage-derived inflammation by inhibiting p38 MAPK activity and might represent a potential novel drug for the treatment of inflammation-related diseases.

ISSN 

0006-291X

Link 

http://dx.doi.org/10.1016/j.bbrc.2018.11.069

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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