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Mesenchymal Stem Cell Regulation of Macrophage Phagocytosis; Quantitation and Imaging
Published on: July 16, 2021
Sulforaphane Regulates Macrophage M1/M2 Polarization to Attenuate Macrophage-induced Caco-2 Cell Injury in an
Ting Yi1, Zhiyin Liu2, Haokun Jia1
1Department of Hematology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Background:
The imbalance between M1 and M2 macrophage activation is closely associated with the pathogenesis of inflammatory bowel diseases (IBDs). Sulforaphane (SFN) plays an important role in the treatment of inflammatory diseases.
Objective:
To investigate the effect of SFN on macrophage polarization and its underlying regulatory mechanism.
Methods:
Mouse bone marrow-derived macrophages (BMDMs) were treated with SFN and an Nrf2 inhibitor, Brusatol. M1 macrophages were induced by LPS and IFN-γ stimulation, whereas M2 macrophages were induced by stimulation with IL-4 and IL-13. LPS-stimulated BMDMs were co-cultured with Caco-2 cells. Flow cytometry, qRT-PCR, and Western blot were performed to assess macrophage polarization. Cell function was assessed using CCK8 assay, transepithelial electrical resistance (TEER) assay, and biochemical analysis.
Results:
Higher concentrations of SFN resulted in better intervention effects, with an optimal concentration of 10 μM. SFN decreased the levels of IL-12, IL-6, and TNF-α, as well as the percentages of CD16/32 in M1 BMDMs. At the same time, SFN increased the levels of YM1, Fizz1, and Arg1 as well as the percentages of CD206+ cells in M2 BMDMs. In addition, SFN enhanced the accumulation of Nrf2, NQO1, and HO-1 in M1 BMDMs, and the downregulation of Nrf2 reversed the regulatory effect of SFN on M1/M2 macrophages. LPS-stimulated BMDMs induced Caco-2 cell damage, which was partially alleviated by SFN.
Conclusion:
Our findings indicate that SFN may act as an Nrf2 agonist to regulate macrophage polarization from M1 to M2. Furthermore, SFN may represent a potential protective ingredient against IBD.
Insights
Sulforaphane (SFN) shifts macrophage polarization from M1 to M2, potentially treating inflammatory bowel diseases (IBD). This occurs via Nrf2 activation, reducing inflammatory markers and improving gut barrier function.
Area of Science:
- Immunology
- Molecular Biology
- Gastroenterology
Background:
- Macrophage polarization imbalance (M1/M2) is key in inflammatory bowel diseases (IBD) pathogenesis.
- Sulforaphane (SFN) shows promise in treating inflammatory conditions.
Purpose of the Study:
- To determine SFN's effect on macrophage polarization.
- To elucidate the regulatory mechanisms of SFN's action.
Main Methods:
- Mouse bone marrow-derived macrophages (BMDMs) were polarized to M1 or M2 phenotypes.
- SFN treatment and Nrf2 inhibition were applied.
- Macrophage polarization was assessed via flow cytometry, qRT-PCR, and Western blot.
- Cell function and gut barrier integrity were evaluated.
Main Results:
- SFN (optimal 10 μM) promoted M2 polarization and suppressed M1 markers (IL-12, IL-6, TNF-α).
- SFN increased M2 markers (YM1, Fizz1, Arg1, CD206+) and Nrf2 pathway activation (Nrf2, NQO1, HO-1).
- Nrf2 inhibition reversed SFN's polarization effects; SFN partially protected Caco-2 cells from LPS-induced damage.
Conclusions:
- SFN acts as an Nrf2 agonist, promoting M2 macrophage polarization.
- SFN demonstrates potential as a therapeutic agent for IBD by modulating macrophage balance and protecting the gut barrier.
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