PMID- 38314669
OWN - NLM
STAT- MEDLINE
DCOM- 20240313
LR  - 20240313
IS  - 1735-367X (Electronic)
IS  - 1735-1383 (Linking)
VI  - 21
IP  - 1
DP  - 2024 Mar 12
TI  - Sulforaphane Regulates Macrophage M1/M2 Polarization to Attenuate 
      Macrophage-induced Caco-2 Cell Injury in an Inflammatory Environment.
PG  - 37-52
LID - 10.22034/iji.2024.98644.2580 [doi]
AB  - 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-gamma 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 muM. SFN decreased the levels of 
      IL-12, IL-6, and TNF-alpha, 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.
FAU - Yi, Ting
AU  - Yi T
AUID- ORCID: 0009-0001-4586-2769
AD  - Department of Hematology, The Affiliated Changsha Central Hospital, Hengyang 
      Medical School, University of South China, Changsha, Hunan, China.
FAU - Liu, Zhiyin
AU  - Liu Z
AUID- ORCID: 0009-0006-2348-1873
AD  - Department of Medical Administration, The Affiliated Changsha Central Hospital, 
      Hengyang Medical School, University of South China, Changsha, Hunan, China.
FAU - Jia, Haokun
AU  - Jia H
AUID- ORCID: 0009-0003-6333-0664
AD  - Department of Hematology, The Affiliated Changsha Central Hospital, Hengyang 
      Medical School, University of South China, Changsha, Hunan, China.
FAU - Liu, Qiongzhi
AU  - Liu Q
AUID- ORCID: 0009-0009-9332-2730
AD  - Department of Hematology, The Affiliated Changsha Central Hospital, Hengyang 
      Medical School, University of South China, Changsha, Hunan, China.
FAU - Peng, Jianjiao
AU  - Peng J
AUID- ORCID: 0009-0006-3135-7944
AD  - Department of Hematology, The Affiliated Changsha Central Hospital, Hengyang 
      Medical School, University of South China, Changsha, Hunan, China.
LA  - eng
PT  - Journal Article
DEP - 20240312
PL  - Iran
TA  - Iran J Immunol
JT  - Iranian journal of immunology : IJI
JID - 101282932
RN  - GA49J4310U (sulforaphane)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Sulfoxides)
RN  - 0 (Isothiocyanates)
SB  - IM
MH  - Mice
MH  - Humans
MH  - Animals
MH  - Caco-2 Cells
MH  - *Macrophage Activation
MH  - *Lipopolysaccharides/pharmacology
MH  - NF-E2-Related Factor 2/pharmacology
MH  - Macrophages
MH  - *Sulfoxides
MH  - *Isothiocyanates
OTO - NOTNLM
OT  - Inflammatory Bowel Disease
OT  - Macrophage
OT  - Nrf2/ARE
OT  - Sulforaphane
EDAT- 2024/02/05 06:43
MHDA- 2024/03/13 06:47
CRDT- 2024/02/05 05:52
PHST- 2024/03/13 06:47 [medline]
PHST- 2024/02/05 06:43 [pubmed]
PHST- 2024/02/05 05:52 [entrez]
AID - 10.22034/iji.2024.98644.2580 [doi]
PST - epublish
SO  - Iran J Immunol. 2024 Mar 12;21(1):37-52. doi: 10.22034/iji.2024.98644.2580.