Nitroalkene inhibition of pro-inflammatory macrophage effector function via modulation of signaling metabolite levels.

ABSTRACT:

Introduction

Classically activated innate immune cells undergo a metabolic switch to aerobic glycolysis to support effector function. We report that the small-molecule nitroalkene 10-n-octadec-9-enoic acid (NO₂-OA) attenuates the Warburg- like phenotype of aerobic glycolysis in lipopolysaccharide (LPS)-activated macrophages, thus inhibiting pro-inflammatory signaling.

Methods

RAW264.7 and bone marrow derived macrophage were treated with LPS with and without NO₂-OA or 1400W. Pro-inflammatory cytokines were measured by ELISA and protein expression was determined by immunoblot. Central carbon metabolites with and without ¹³C stable isotope tracing were measured using liquid chromatography-high resolution mass spectrometry.

Results

Overall

SUBMITTER: Stevenson ER 

PROVIDER: S-EPMC12572803 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature