A novel pharmacologic inhibitor of the NLRP3 inflammasome limits myocardial injury after ischemia-reperfusion in the mouse.

ABSTRACT:

Background

The formation of the NLRP3 inflammasome in the heart during acute myocardial infarction amplifies the inflammatory response and mediates further damage. Glyburide has NLRP3 inhibitory activity in vitro but requires very high doses in vivo, associated with hypoglycemia. The aim of this study was to measure the effects on the NLRP3 inflammasome of 16673-34-0, an intermediate substrate free of the cyclohexylurea moiety, involved in insulin release.

Methods and results

We synthesized 16673-34-0 (5-chloro-2-methoxy-N-[2-(4-sulfamoylphenyl)ethyl]benzamide) that displayed no effect on glucose metabolism. HL-1 cardiomyocytes were treated with lipopolysaccharide and ATP to induce the formation of the NLRP3 inflammasome, measured as increased caspase-1 activity and cell dea

SUBMITTER: Marchetti C 

PROVIDER: S-EPMC3980088 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature