Docosahexaenoic acid enhances M2 macrophage polarization via the p38 signaling pathway and autophagy

2019 ◽  
Vol 120 (8) ◽  
pp. 12604-12617 ◽  
Author(s):  
Aki Kawano ◽  
Wataru Ariyoshi ◽  
Yoshie Yoshioka ◽  
Hisako Hikiji ◽  
Tatsuji Nishihara ◽  
...  
Keyword(s):  
Docosahexaenoic Acid ◽  
Signaling Pathway ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization

scholarly journals Convallatoxin Promotes M2 Macrophage Polarization to Attenuate Atherosclerosis Through PPARγ-Integrin αvβ5 Signaling Pathway

2021 ◽  
Vol Volume 15 ◽  
pp. 803-812
Author(s):  
Yi Zhang ◽  
Xiujin Shi ◽  
Jialun Han ◽  
Wenxing Peng ◽  
Zhenwei Fang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization

Ginsenoside Rg1 Ameliorated Colitis by Regulating the Homeostasis of M1/M2 Macrophage Polarization and Intestinal Flora

2021 ◽  
Author(s):  
Jian Long ◽  
Xue-Ke Liu ◽  
Zeng-Ping Kang ◽  
Meng-Xue Wang ◽  
Hai-Mei Zhao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Macrophage Activation ◽  
Macrophage Polarization ◽  
Intestinal Flora ◽  
M2 Macrophage ◽  
Ginsenoside Rg1 ◽  
Tnf Α ◽  
M2 Macrophage Polarization ◽  
Rhoa Signaling

Abstract Background: Aberrant M1/M2 macrophage polarization and intestinal flora disruption are involved in the pathological processes associated with ulcerative colitis (UC). Ginsenoside Rg1 has good immunomodulatory and anti-inflammatory effects and is effective in treating UC of humans and animals. However, it is unclear how ginsenoside Rg1 regulate the homeostasis of M1/M2 macrophage polarization and intestinal flora.Methods: BALB/c mice were randomly divided into 4 groups: Control, DSS, DSS+Rg1, DSS+Y27632 groups. In this study, experiment colitis was induced in BALB/c mice using sodium dextran sulfate (DSS). Mice of DSS+Rg1, DSS+Y27632 groups were treated respectively with ginsenoside Rg1 and Rock inhibitor Y27632 for 14 consecutive days. On day 21, all mice were sacrificed. Histopathological analysis of the colon tissues was performed by Hematoxylin Eosin sinning. Cytokines (IL-6, IL-33, CCL-2, TNF-α, IL-4 and IL-10) were detected by Elisa. Flow cytometry was used to analyse macrophage activation and M1/M2 macrophage polarisation. Western blotting were applied to detect the levels of Macrophage polarization-associated protein (Arg-1, MIF-1, PIM-1, TLR2) and Nogo-B/RhoA signaling molecules (Rock1, RhoA and Nogo-B). The fecal microbial populations were analyzed using 16S gene sequencing. Results: After ginsenoside Rg1 and Y27632 treatment, the changes of body weight, colon length, colonic weight index and colonic mucosal injury of colitis mice were effectively improved, accompanied by less ulcer formation and inflammatory cell infiltration, lower levels of pro-inflammatory cytokines (IL-6, IL-33, CCL-2, TNF-α) and higher anti-inflammatory cytokines (IL-4 and IL-10). Importantly, the percentage of CD11b+F4/80+, CD11b+F4/80+Tim-1+, CD11b+F4/80+TLR4+, and CD11b+F4/80+iNOS+ cells and the expression levels of MIF-1 and PIM-1 proteins were down-regulated significantly after ginsenoside Rg1 and Y27632 treatment, and CD11b+F4/80+CD206+ and CD11b+F4/80+CD163+ cells and Arg-1 up-regulated significantly. Intestinal flora composition were effectively improved after administration of ginsenoside Rg1. The Nogo-B/RchoA signaling pathway were obviously inhibited after ginsenoside Rg1 and Y27632 treatment, and the levels of Rock1, RhoA and Nogo-B proteins were significantly reduced. Conclusions: Ginsenoside Rg1 has the protective effect on UC by inhibiting macrophage activation, restoring the balance of M1/M2 macrophage polarization, and improving intestinal flora composition, associated with inhibition of the Nogo-B/RhoA signaling pathway.

scholarly journals Transcriptome profiling reveals new insights into the roles of neuronal nitric oxide synthase on macrophage polarization towards classically activated phenotype

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257908
Author(s):  
Pingan Chang ◽  
Hao Gao ◽  
Quan Sun ◽  
Xiaohong He ◽  
Feifei Huang
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Macrophage Polarization ◽  
Neuronal Nitric Oxide Synthase ◽  
M2 Macrophage ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization ◽  
Oxide Synthase ◽  
First Time ◽  
Classically Activated

In response to various stimuli, naïve macrophages usually polarize to M1 (classically activated) or M2 (alternatively activated) cells with distinct biological functions. Neuronal nitric oxide synthase (NOS1) is involved in M1 macrophage polarization at an early stage. Here, we show for the first time that NOS1 is dispensable for M2 macrophage polarization for the first time. Further, differentially expressed genes (DEGs) regulated by NOS1 signaling in M1-polarized macrophages stimulated with lipopolysaccharide (LPS) were characterized by transcriptome analysis of wild-type (WT) and NOS1 knockout mouse macrophages. Thousands of affected genes were detected 2 h post LPS challenge, and this wide-ranging effect became greater with a longer stimulation time (8 h post LPS). NOS1 deficiency caused dysregulated expression of hundreds of LPS-responsive genes. Most DEGs were enriched in biological processes related to transcription and regulation of the immune and inflammatory response. At 2 h post-LPS, the toll-like receptor (TLR) signaling pathway, cytokine–cytokine receptor interaction, and NOD-like receptor signaling pathway were the major pathways affected, whereas the main pathways affected at 8 h post-LPS were Th1 and Th2 cell differentiation, FoxO, and AMPK signaling pathway. Identified DEGs were validated by real-time quantitative PCR and interacted in a complicated signaling pathway network. Collectively, our data show that NOS1 is dispensable for M2 macrophage polarization and reveal novel insights in the role of NOS1 signaling at different stages of M1 macrophage polarization through distinct TLR4 plasma membrane-localized and endosome-internalized signaling pathways.

scholarly journals Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Zeng-Ping Kang ◽  
Meng-Xue Wang ◽  
Tian-Tian Wu ◽  
Duan-Yong Liu ◽  
Hai-Yan Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Signaling Pathway ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Macrophage Polarization ◽  
Experimental Colitis ◽  
The Body ◽  
M2 Macrophage ◽  
Therapeutic Effects ◽  
M2 Macrophage Polarization

Curcumin has shown good efficacy in mice with experimental colitis and in patients with ulcerative colitis, but the mechanism of action through the regulation of M1/M2 macrophage polarization has not been elaborated. The ulcerative colitis was modeled by dextran sulfate sodium; colitis mice were orally administrated with curcumin (10 mg/kg/day) or 5-ASA (300 mg/kg/day) for 14 consecutive days. After curcumin treatment, the body weight, colon weight and length, colonic weight index, and histopathological damage in colitis mice were effectively improved. The concentrations of proinflammatory cytokines IL-1β, IL-6, and CCL-2 in the colonic tissues of colitis mice decreased significantly, while anti-inflammatory cytokines IL-33 and IL-10 increased significantly. Importantly, macrophage activation was suppressed and M1/M2 macrophage polarization was regulated in colitis mice, and the percentage of CD11b+F4/80+ and CD11b+F4/80+TIM-1+ and CD11b+F4/80+iNOS+ decreased significantly and CD11b+F4/80+CD206+ and CD11b+F4/80+CD163+ increased significantly. Additionally, curcumin significantly downregulated CD11b+F4/80+TLR4+ macrophages and the protein levels of TLR2, TLR4, MyD88, NF-κBp65, p38MAPK, and AP-1 in colitis mice. Our study suggested that curcumin exerted therapeutic effects in colitis mice by regulating the balance of M1/M2 macrophage polarization and TLRs signaling pathway.

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