Oleuropein reduces LPS-induced inflammation via stimulating M2 macrophage polarization

Mirsanei, Zahra; Heidari, N.; Hazrati, A.; Asemani, Yahya; Niknam, Bahare; Yousefi, Zahra; Jafari, Reza

doi:10.1016/j.biopha.2023.114857

Cited by 14 publications

(4 citation statements)

References 44 publications

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“…Quercetin, a natural flavonoid, has an apparent anti-inflammatory effect by regulating macrophage polarization [8]. Many genes related to macrophage polarization were identified in the screened CSD targets for UC treatment, such as NOS2 (iNOS), CXCL10, TNF-α, IL-6, IL10, and IL-1β [8,35]. Moreover, the biological functions of oxidative stress, Immune response disorder manifests as an imbalance in macrophage polarization, and it is one of the pathogenesis factors of UC, which is important in UC research.…”

Section: Discussionmentioning

confidence: 99%

Compound sophora decoction alleviates ulcerative colitis by regulating macrophage polarization through cGAS inhibition: network pharmacology and experimental validation

Gao,

Deng,

Liu

et al. 2024

Aging

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Introduction: Ulcerative colitis (UC) is a refractory disease with complex pathogenesis, and its pathogenesis is not clear. The present study aimed to investigate the potential target and related mechanism of Compound Sophora Decoction (CSD) in treating UC. Methods: A network pharmacology approach predicted the components and targets of CSD to treat UC, and cell and animal experiments confirmed the findings of the approach and a new target for CSD treatment of UC. Results: A total of 155 potential targets were identified for CSD treatment of UC, with some related to macrophage polarization, such as nitric oxide synthase (NOS2), also known as inducible nitric oxide synthase (iNOS). GO and KEGG enrichment analysis indicated that oxidative stress response and multiple inflammatory signaling pathways such as TNF-α may play a significant role. In vitro experiments revealed that Interferonstimulated DNA (ISD) interference can cause polarization imbalances in Raw 264.7 and bone marrow-derived macrophages (BMDMs). Flow cytometry demonstrated that polarization of macrophages in the intestine, spleen, and lymph nodes in vivo was also unbalanced after dextran sulfate sodium (DSS) modeling with pathological intestinal injury. Both in vitro and in vivo studies indicated that after inducing inflammation, the levels of macrophage polarization-related markers (iNOS and Arg1) and inflammation-related factors (CCL17, IL10, TNF-α, and CXCL10) changed, accompanied by increased expression of cGAS. However, CSD treatment based on inflammation can inhibit the expression of cGAS protein and mRNA, lower the level of inflammatory factors, promote the expression of anti-inflammatory factors, and regulate macrophage polarization. Conclusion: We concluded that CSD alleviated DSS-induced UC by inhibiting cGAS, thus regulating macrophage polarization.

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Section: Discussionmentioning

confidence: 99%

Compound sophora decoction alleviates ulcerative colitis by regulating macrophage polarization through cGAS inhibition: network pharmacology and experimental validation

Gao,

Deng,

Liu

et al. 2024

Aging

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“…RAW 264.7 cells were seeded 6 well plates and treated with vehicle (saline, NaCl 0.9%) (CTRL) or LPS (100 ng/ml) [ 39 , 40 ] and PSELT (5 nM) alone or in co-treatment for 24 h. At the end of the treatments, cells were washed with cold DPBS detached with trypsin–EDTA and centrifuged. The pellet was resuspended in 100 µl of cold DPBS containing FITC anti-CD80 (B7-1) monoclonal antibody (11–0801-82) (Thermo Fisher Scientific) according to the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

The redox-active defensive Selenoprotein T as a novel stress sensor protein playing a key role in the pathophysiology of heart failure

De Bartolo,

Pasqua,

Romeo

et al. 2024

J Transl Med

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Maladaptive cardiac hypertrophy contributes to the development of heart failure (HF). The oxidoreductase Selenoprotein T (SELENOT) emerged as a key regulator during rat cardiogenesis and acute cardiac protection. However, its action in chronic settings of cardiac dysfunction is not understood. Here, we investigated the role of SELENOT in the pathophysiology of HF: (i) by designing a small peptide (PSELT), recapitulating SELENOT activity via the redox site, and assessed its beneficial action in a preclinical model of HF [aged spontaneously hypertensive heart failure (SHHF) rats] and against isoproterenol (ISO)-induced hypertrophy in rat ventricular H9c2 and adult human AC16 cardiomyocytes; (ii) by evaluating the SELENOT intra-cardiomyocyte production and secretion under hypertrophied stimulation. Results showed that PSELT attenuated systemic inflammation, lipopolysaccharide (LPS)-induced macrophage M1 polarization, myocardial injury, and the severe ultrastructural alterations, while counteracting key mediators of cardiac fibrosis, aging, and DNA damage and restoring desmin downregulation and SELENOT upregulation in the failing hearts. In the hemodynamic assessment, PSELT improved the contractile impairment at baseline and following ischemia/reperfusion injury, and reduced infarct size in normal and failing hearts. At cellular level, PSELT counteracted ISO-mediated hypertrophy and ultrastructural alterations through its redox motif, while mitigating ISO-triggered SELENOT intracellular production and secretion, a phenomenon that presumably reflects the extent of cell damage. Altogether, these results indicate that SELENOT could represent a novel sensor of hypertrophied cardiomyocytes and a potential PSELT-based new therapeutic approach in myocardial hypertrophy and HF. Graphical Abstract

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“…During the development of inflammation, changes in glycolytic metabolism led to overproduction of ROS in macrophages, which recruit M1-like pro-inflammatory macrophages [59] . Macrophages are activated in a classical (M1) or non-classical (M2, alternate activation) manner [60] . Type M1 promotes the production of IL-12, IL-23, and nitrite oxide (NO•) to exacerbate the inflammatory response.…”

Section: Lipopolysaccharides (Lps): Inducers Of Inflammationmentioning

confidence: 99%

Beneficial effects of food-derived polyphenols on type 2 diabetes: mechanistic insights based on gut microbiota alterations and anti-inflammatory responses

Song,

Jia

2023

Food Science of Animal Products

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Food-derived polyphenols and their effects on type 2 diabetes are linked to the microbiota. Here, we expound on the mechanisms of food-derived polyphenols that affect the onset of type 2 diabetes, focusing on the roles played by gut microorganisms and the metabolites they produce. We also discuss the mechanism of food-derived polyphenols lower blood glucose through host signaling-mediated inflammatory responses. Food-derived polyphenols alleviate the development of type 2 diabetes by remodeling gut microbiome composition and reducing inflammatory responses. Food-derived polyphenols inhibit the activity of α-glucosidase, α-amylase, and dipeptidyl peptidase IV enzymes to reduce postprandial blood glucose levels. The nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) is considered a key regulator of food-derived polyphenols in alleviating the onset of type 2 diabetes. Inhibition of NF-κB activation can increase insulin sensitivity, reduce inflammation, and maintain glucose homeostasis. This investigation reveals that food-derived polyphenols can alleviate the onset of type 2 diabetes and offers adequate theoretical knowledge in support of their usage as such.

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Oleuropein reduces LPS-induced inflammation via stimulating M2 macrophage polarization

Cited by 14 publications

References 44 publications

Compound sophora decoction alleviates ulcerative colitis by regulating macrophage polarization through cGAS inhibition: network pharmacology and experimental validation

Compound sophora decoction alleviates ulcerative colitis by regulating macrophage polarization through cGAS inhibition: network pharmacology and experimental validation

The redox-active defensive Selenoprotein T as a novel stress sensor protein playing a key role in the pathophysiology of heart failure

Beneficial effects of food-derived polyphenols on type 2 diabetes: mechanistic insights based on gut microbiota alterations and anti-inflammatory responses

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