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.

KEYWORDS:

• Bone marrow-derived macrophages
• high glucose
• macrophage polarization
• mogroside V
• NF-κB
• p38 MAPK

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The data sets used and/or analyzed during the current study are available from the corresponding author on reasonable request [email protected].

Supplementary material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/08820139.2024.2321353.

Author contributions

HL and XD designed the research study. XD, ZY, CL, KL, XZ and HL acquired the data. XD and ZY analyzed the data. XD, ZY and CL interpreted the data. HL provided help and advice on acquisition, analysis and interpretation of the data. XD and ZY wrote the manuscript. HL, CL, KL and XZ reviewed the manuscript critically for important intellectual content. All authors contributed to editorial changes in the manuscript. All authors read and approved the final manuscript.

Additional information

Funding

This research was supported by National Natural Science Foundation of China (82060195), Joint Project on Regional High-Incidence Diseases Research of Guangxi Natural Science Foundation (2023GXNSFAA026264), Nanning Qingxiu District Science and Technology Plan (2021002) and Innovation Project of Guangxi Graduate Education (YCSW2023234).