Gallic acid Inhibits M1 Macrophage Polarization via Adenosine 5’-Monophosphate-Activated Protein Kinase/Signal Transducers and Activators of Transcription 1 Pathway

To investigate the role of gallic acid in lipopolysaccharide/interferon-gamma induced macrophage polarization toward M1. Macrophages were isolated from peritoneal wash fluid and exposed to prepared at concentrations control, 6.25, 12.5, 25 37.5 μg/ml, presence lipopolysaccharide interferon-gamma, for establishment M1 polarization. Adenosine 5’-monophosphate-activated protein kinase inhibitor compound C was used pre-treat macrophages; cell viability determined by flow cytometry with Annexin V-PE/7-amino actinomycin D staining, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide trypan blue assays; applied evaluate expression F4/80+ inducible nitric oxide synthase+ real-time polymerase chain reaction assess messenger ribonucleic level synthase, tumor necrosis factor-alpha interleukin-1beta. Protein levels cyclooxygenase-2, adenosine 5‘-monophosphate-activated kinase, signal transducers activators transcription 1 phosphorylation evaluated Western blotting. Gallic 6.25-37.5 μg/ml showed no noticeable effects on macrophages viability, but significantly decreased factoralpha, interleukin-1 beta, cyclooxygenase-2 phospho-signal 1, meanwhile increased p-adenosine contents a concentration-dependent manner. pre-treatment can reverse may inhibit via kinase/signal signaling pathway.