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Title 

JH-reduces HMGB1-mediated septic responses and improves survival rate in septic mice

Authors 

Wonhwa LeeO YuseokS YangB S LeeJ H LeeE K ParkM C BaekG Y SongJ S Bae

Publisher 

Wiley

Issue Date 

2019

Citation 

Journal of Cellular Biochemistry

Keywords 

JH-4endotheliumhigh mobility group box 1 (HMGB1)sepsis

Abstract 

Inhibition of high mobility group box 1 (HMGB1) and restoration of endothelial integrity are emerging as attractive therapeutic strategies for the management of severe vascular inflammatory diseases. Recently, we found that JH-4, a synthesized decursin derivative, exhibited a strong anti-Hutchinson-Gilford progeria syndrome by efficiently blocking progerin-lamin A/C binding. In this study, we examined the effects of JH-4 on HMGB1-mediated septic responses and the survival rate in a mouse sepsis model. The anti-inflammatory activities of JH-4 were monitored based on its effects on lipopolysaccharide- or cecal ligation and puncture (CLP)-mediated release of HMGB1. The antiseptic activities of JH-4 were determined by measuring permeability, leukocyte adhesion, migration, and the activation of proinflammatory proteins in HMGB1-activated human umbilical vein endothelial cells and mice. JH-4 inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses in human endothelial cells. JH-4 also inhibited HMGB1-mediated hyperpermeability and leukocyte migration in mice. In addition, treatment with JH-4 reduced CLP-induced release of HMGB1, sepsis-related mortality, and pulmonary injury in vivo. Our results indicate that JH-4 is a possible therapeutic agent to treat various severe vascular inflammatory diseases via the inhibition of the HMGB1 signaling pathway.

URI 

https://doi.org/10.1002/jcb.27914

ISSN 

0730-2312

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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