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Nicotinic acid inhibits NLRP3 inflammasome activation via SIRT1 in vascular endothelial cells.

Abstract：

:Emerging evidences indicated that NLRP3 inflammasome initiates inflammatory response involved in cardiovascular disease. Nicotinic acid (NA) has been known to possess potential anti-inflammatory property. The aim of this study was to investigate the effect of NA on the activation of NLRP3 inflammasome and the underlying mechanisms. It was found that lipopolysaccharide (LPS) and adenosine triphosphate (ATP) triggered the activation of NLRP3 inflammasome in human umbilical vein endothelial cells (HUVECs). NA inhibited NLRP3 inflammasome activation and subsequent caspase-1 cleavage as well as interleukin (IL)-1β secretion. Moreover, NA administration up-regulated SIRT1 expression in HUVECs stimulated with LPS plus ATP. Importantly, knockdown of SIRT1 reversed the inhibitory effect of NA on the activation of NLRP3 inflammasome. Further study revealed that NA also decreased the generation of reactive oxygen species (ROS) in HUVECs. In addition, NA inhibited NLRP3 inflammasome activation partly through suppression of ROS. Taken together, these findings indicate that NA is able to regulate the activation of NLRP3 inflammasome in HUVECs, which may be partly mediated by SIRT1 and ROS.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Li Y,Yang G,Yang X,Wang W,Zhang J,He Y,Zhang W,Jing T,Lin R

doi

10.1016/j.intimp.2016.09.003

subject

Has Abstract

pub_date

2016-11-01 00:00:00

pages

211-218

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(16)30378-2

journal_volume

40

pub_type

杂志文章

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