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Cilostazol inhibits HMGB1 release in LPS-activated RAW 264.7 cells and increases the survival of septic mice.

Abstract：

INTRODUCTION:Inflammation and coagulation play important roles in the pathogenesis of sepsis. Anticoagulants with anti-inflammatory action draw attention as therapeutic agent in sepsis. OBJECTIVE:Whether cilostazol (6-[4-(1-cyclohexyl-1H-tetrazol-5-yl) butoxy]-3,4-dihydro-2-(1H)-quinolinone), anticoagulant, protects mice against sepsis and underlying mechanism(s) were investigated. METHODS:Induction of heme oxygenase (HO)-1 protein, phosphorylation of 5' adenosine monophosphate-activated protein kinase (AMPK), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) luciferase activity, and release of high mobility group box 1 (HMGB1) were analyzed using signal inhibitors and transfection techniques. Survival and organ damage were compared in septic mice with and without cilostazol. RESULTS:In RAW264.7 cells, cilostazol increased phosphorylation of AMPK which was followed by HO-1 induction. Lipopolysaccharide (LPS)-activated HMGB1 release was reduced by cilostazol which was reversed by both SB203580 and silencing of HO-1 or AMPK RNA. Interestingly, silencing AMPK reduced HO-1 expression, whereas silencing HO-1 did not affect p-AMPK by cilostazol. Both compound C and zinc protoporphyrin IX (ZnPPIX) antagonized inhibitory effect of HMGB1 by cilostazol. Cilostazol inhibited NF-κB luciferase activity which was antagonized by SB203580. Finally, the administration of cilostazol increased the survival of endotoxemic mice but failed to do so when co-treated with rHMGB1. Cilostazol reduced circulating HMGB1, plasminogen activator inhibitor-1 (PAI-1) levels, organ damages and protein expression of PAI-1 in lung tissues of CLP-septic mice, which were antagonized by ZnPPIX. CONCLUSION:These findings suggest that HMGB1 can be a target molecule of cilostazol by 1) AMPK activation, and 2) induction of HO-1 by p38 MAPK and AMPK. Therefore, cilostazol may be useful for treatment of sepsis.

journal_name

Thromb Res

journal_title

Thrombosis research

authors

Chang KC

doi

10.1016/j.thromres.2015.06.017

subject

Has Abstract

pub_date

2015-08-01 00:00:00

pages

456-64

issue

2

eissn

0049-3848

issn

1879-2472

pii

S0049-3848(15)30030-X

journal_volume

136

pub_type

杂志文章

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