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Attenuation of pristimerin on TNF-α-induced endothelial inflammation.

Abstract：

OBJECTIVE:Pristimerin is known to have anti-cancer and anti-inflammatory activities; however, its therapeutic mechanism has not been described. In this study, to investigate the therapeutic mechanism of pristimerin, we examined the effect of pristimerin on TNF-α-induced endothelial inflammatory response both in vitro and in vivo. METHODS:Leukocyte-endothelium Adhesion Assay was use to evaluate the endothelial cell-monocyte interaction. Western blotting was used to confirm protein expression. NF-κB p65 nuclear translocation in endothelial cells was detected using immunofluorescent microscopy. In vivo leukocyte infiltration was evaluated using acute lung inflammation model. RESULTS:Pristimerin profoundly inhibited TNF-α-induced adhesion of monocytes to human endothelial cells and the leukocyte transmigration. Pristimerin dramatically inhibited the expression of TNF-α-induced endothelial adhesion molecules (intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)) and the pro-inflammatory cytokine (IL-6, IL-8 and monocyte chemoattractant protein-1 (MCP-1)). Pristimerin suppressed the penetration of the leukocyte in the acute lung injury mice model. Furthermore, pristimerin also suppressed the TNF-α-activated Nuclear factor kappa B (NF-κB) activation. CONCLUSIONS:Pristimerin has the anti-inflammatory properties in endothelial cells, at least in part, through the suppression of NF-κB activation, which may have a potential therapeutic effects for inflammatory vascular diseases.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Liang J,Yuan S,Wang X,Lei Y,Zhang X,Huang M,Ouyang H

doi

10.1016/j.intimp.2020.106326

subject

Has Abstract

pub_date

2020-03-02 00:00:00

pages

106326

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(19)32706-7

journal_volume

82

pub_type

杂志文章

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