Related Experiment Video
Updated: May 5, 2026

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
Monomethyl Branched-Chain Fatty Acids Suppress M1 Macrophage Polarization via FABP4/PPAR-γ Signaling Pathway
Yuan He1, Yu Zhang1, Shuang Zhu1
1State Key Laboratory of Food Science and Resources, School of Food Science and Technology, National Engineering Reacher Center for Functional Food, National Engineering Laboratory for Cereal Fermentation Technology, Collaborative Innovation Center of Food Safety and Quality Control in Jiangsu Province, Jiangnan University, No. 1800, Lihu Road, Wuxi, Jiangsu, 214122, People's Republic of China.
Scope:
Monomethyl-branched chain fatty acids (mmBCFAs) are found in a variety of food sources and are of great interest due to their potent antiinflammatory properties. However, most of the current researches have concentrated on the relationship between mmBCFAs and intestinal inflammation, and there is a large gap in the biological mechanisms involved behind their antiinflammatory effects.
Methods And Results:
The present study examines the role of mmBCFAs in modulating macrophage polarization. The results demonstrate that iso-C16:0 significantly inhibits macrophages M1 proinflammatory polarization through regulating FABP4/PPAR-γ pathway. Proteomics and molecular biology experiments verify that metabolic reprogramming is involved in the inhibition of M1 macrophage, referring to the upregulation of fatty acid oxidation, TCA cycle, and oxidative phosphorylation, as well as downregulation of glycolytic flux.
Conclusion:
In summary, this study offers a novel perspective on the antiinflammatory effects mediated by mmBCFAs.
More Related Videos
07:45Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis
Published on: November 28, 2015
07:46Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017