Mogroside Ⅴ Inhibits M1 Polarization and Inflammation of Diabetic Mouse Macrophages via p38 MAPK/NF-Κb Signaling Pathway.

Abstract

Background: Mogroside V (MV) has anti-inflammatory properties. However, its impact on macrophage polarization under diabetic condition is yet unclear. This study aimed to investigate effects and underlying mechanisms of MV on inflammatory response and M1 polarization of bone marrow-derived macrophages (BMDMs) from diabetic mice.

Methods: BMDMs were isolated from normal and diabetic C57BL/6 mice. LPS and IFN-γwere used to produce M1-polarized BMDMs. MV treatment was administered throughout the M1 polarization process with or without SB203580 or PDTC. Surface markers CD11b, F4/80 and CD86 of macrophages were identified using flow cytometry or immunofluorescence staining. Inflammatory cytokines IL-1β and IL-6 and phosphorylation levels of p65 and p38 were examined by western blot.

Results: High glucose increased proportion of CD11b⁺F4/80⁺CD86⁺ cells, protein levels of inflammatory cytokines IL-1β and IL-6 and phosphorylation levels of p65 and p38 in LPS+IFN-γ-induced BMDMs, while they were decreased upon MV treatment. Additionally, these effects were further downregulated when MV was co-added with SB203580 or PDTC.

Conclusions: MV suppressed M1 macrophage polarization and inflammatory response, which was partially through NF-κB and p38 MAPK in LPS+IFN-γ induced BMDMs under high glucose condition, implying the potential of MV in treatment for inflammatory complications of diabetes.