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Abstract

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

Author(s): Hexin Mao, Ning Guan, Xiuqiu Gao, Wenjuan Zhang, Gaofeng Xue and Linyuan Wang*
Department of Periodontics, School of Stomatology of Jinzhou Medical College, 1Key Laboratory of Brain and Spinal Cord Injury, First Affiliated Hospital, Jinzhou Medical University, Linghe, Jinzhou 121000, China

Correspondence Address:
Linyuan Wang, Department of Periodontics, School of Stomatology of Jinzhou Medical College, Linghe, Jinzhou 121000, China, E-mail: [email protected]


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

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