Galectin-3 Attenuates Lipopolysaccharides-induced Inflammation in Adipocyte and Macrophage Co-culture System

Abstract

Introduction: Galectin-3 (Gal-3) expression act as a potential novel therapeutic strategy in the treatment of a broad range of inflammatory diseases. Aim: This study aims to study the cross-talk between macrophage and adipocyte cells with Gal-3 upon lipopolysaccharides (LPSs) challenge. Materials and Methods: Cytokine secretion in 3T3-L1 adipocyte-RAW 264.7 macrophage cells were greatly enhanced on LPS stimulation compared to isolated cell culture system, suggesting the cross-talk between these cell types during LPS exposure. Gene and protein expression profile was analyzed by reverse transcription-polymerase chain reaction for understanding the inflammatory responses. Results: Decreased expression of interleukin 6 was confirmed as lowered suppressor of cytokine signaling 3 expressions downstream. A critical appraisal of the role of nuclear factor-κB (NF-κB) in LPS induced alteration of inflammatory phenotype was confirmed as decreased formation of tumor necrosis factor-α transcript using specific inhibitors of NF-κB, along with LPS treatment. Further, Gal-3 also inhibited nuclear p65 translocation, IkB-α degradation and induction of inducible nitric oxide synthase, in response to LPS. Conclusion: These results clearly suggest decreased oxidative burden and inflammation are significantly affected by Gal-3.