Abstract: Objective: The aim of this study was to explore the anti-inflammatory effect of (-)-epigallocatechin gallate (EGCG) and its effects on macrophage polarization. Methods: Primary cultures of mouse peritoneal macrophages were divided into 4 groups: control, 1 μg/mL lipopolysaccharides (LPS), 25 μmol/L EGCG, and 25 μmol/L EGCG + 1 μg/mL LPS groups. Flow cytometry analysis was used to determine phagocytosis, reactive oxygen species (ROS) and apoptosis. Cell proliferation was monitored by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. NO generation was analyzed by Griess method. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were determined by enzyme linked immunosorbent assay (ELISA). The expression of Toll-like receptor 4 (TLR4) and NF-κB p65 proteins was detected by using Western blot analysis. Results: EGCG and/or LPS were no significant effect on cell proliferation or apoptosis in mouse peritoneal macrophages. Compared with the LPS group, EGCG could significantly inhibit the LPS-induced increasing in ROS, NO, TNF-α and IL-1β in peritoneal macrophages (P < 0.01), thereby consequently suppress the polarization of macrophages into M1 phenotype and consequently exerting anti-inflammatory effects. Compared with the LPS group, the expression of TLR4 protein in macrophages and the expression of nuclear transcription factor-κB (NF-κB) p65 in nucleus were significantly decreased in the EGCG + LPS group (P < 0.01). Conclusion: EGCG could inhibit LPS-induced inflammatory responses in mouse peritoneal macrophages, and the underlying mechanism may be related to the blocking of the polarization of macrophages into M1 phenotype via the TLR4-mediated NF-κB pathway.

Key words: (-)-epigallocatechin gallate, anti-inflammatory effects, cell phenotype, NF-κB pathway, macrophage polarization