scholarly journals Immunostimulatory activity and anti-obesity activity of Hibiscus manihot leaves in mouse macrophages, RAW264.7 cells and mouse adipocytes, 3T3-L1 cells

2021 ◽  
Vol 87 ◽  
pp. 104803
Author(s):  
Na Gyeong Geum ◽  
Ju-Hyeong Yu ◽  
Joo Ho Yeo ◽  
Min Yeong Choi ◽  
Jae Won Lee ◽  
...  
Keyword(s):  
Raw264.7 Cells ◽  
Immunostimulatory Activity ◽  
Mouse Macrophages ◽  
Mouse Adipocytes

scholarly journals Rice sprouts exert immunostimulatory activity in mouse macrophages, RAW264.7 cells

2021 ◽  
Vol 32 (1) ◽  
pp. 349-359
Author(s):  
Na Gyeong Geum ◽  
Joo Ho Yeo ◽  
Ju Hyeong Yu ◽  
Min Yeong Choi ◽  
Jae Won Lee ◽  
...  
Keyword(s):  
Raw264.7 Cells ◽  
Immunostimulatory Activity ◽  
Mouse Macrophages

scholarly journals Phenolic Compounds and Ginsenosides in Ginseng Shoots and Their Antioxidant and Anti-Inflammatory Capacities in LPS-Induced RAW264.7 Mouse Macrophages

2019 ◽  
Vol 20 (12) ◽  
pp. 2951 ◽  
Author(s):  
Fan Yao ◽  
Qiang Xue ◽  
Ke Li ◽  
Xinxin Cao ◽  
Liwei Sun ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Phenolic Compounds ◽  
High Performance ◽  
Raw264.7 Cells ◽  
Inflammatory Factors ◽  
Tnf Α ◽  
Mouse Macrophages ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
First Time

We conducted this study for the first time to evaluate changes in the composition and contents of phenolic compounds and ginsenosides in ginseng shoot extracts (GSEs) prepared with different steaming times (2, 4, and 6 h) at 120 °C, as well as their antioxidant and anti-inflammatory activities in lipopolysaccharide (LPS)-induced RAW264.7 mouse macrophages (RAW264.7 cells). The results show that total phenol and flavonoid contents were both significantly higher in steamed versus raw GSEs, and the same trend was found for 2,2′-diphenyl-1-picrylhydrazyl (DPPH•) and 2,2′-azobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS•+) scavenging capacities. Among the 18 ginsenosides quantified using high-performance liquid chromatography (HPLC) with the aid of pure standards, polar ginsenosides were abundant in raw GSEs, whereas less-polar or rare ginsenosides appeared after steaming at 120 °C and increased with steaming time. Furthermore, steamed GSEs exhibited a greater ability to inhibit the production of inflammatory mediators and pro-inflammatory cytokines, such as nitric oxide (NO), interleukin (IL)-6, and tumor necrosis factor (TNF)-α in LPS-induced RAW264.7 cells at the same concentration. Relative expression levels of inducible nitric oxide synthase (iNOS), IL-6, TNF-α, and cyclooxygenase-2 (COX-2) mRNAs were attenuated by the GSEs, probably due to the enrichment of less-polar ginsenosides and enhanced antioxidant activity in steamed GSEs. These findings, combined with correlation analysis, showed that less-polar ginsenosides were major contributors to the inhibition of the overproduction of various inflammatory factors, while the inhibitory effects of total phenols and total flavonoids, and their antioxidant abilities, are also important.

Role of Brd4 in the production of inflammatory cytokines in mouse macrophages treated with titanium particles

2019 ◽  
Vol 97 (11) ◽  
pp. 1028-1034 ◽  
Author(s):  
Yuanzhong Ren ◽  
Yongtao Zhang ◽  
Ze Wang ◽  
Changyao Wang ◽  
Haining Zhang ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Wear Particle ◽  
Raw264.7 Cells ◽  
Inflammatory Cytokine Production ◽  
Tnf Α ◽  
Mouse Macrophages ◽  
Ti Particles

Brd4 protein is an important epigenetic regulator involved in the process of inflammatory cytokine production in many diseases. However, whether and how Brd4 participates in the process of wear-particle-induced inflammation remain unclear. This study aimed to investigate the potential role of Brd4 in titanium (Ti) particle-induced inflammatory cytokine production in mouse macrophage RAW264.7 cells. Our experiment detected Brd4 expressed in both normal synovium and periprosthetic osteolysis interface membrane, but the expression increased in the interface membrane as compared with that in normal synovium. Treatment with Ti particles significantly increased TNF-α, IL-6, and IL-1β production in RAW264.7 cells, which was inhibited by JQ1 or Brd4-siRNA. Ti particles enhanced the expression of Brd4, which was abrogated by JQ1. Ti particles enhanced NF-κB p65 and IKK phosphorylation and attenuated IκBα protein expression, which were abrogated by JQ1. Co-immunoprecipitation analysis indicated that Ti particles promoted the binding of Brd4 to acetylated NF-κB p65 (lysine-310), which was also abrogated in JQ1-treated RAW264.7 cells. In conclusion, Brd4 expression increases in interface membrane and Brd4 participates in the production of pro-inflammatory cytokines induced by Ti particles via promoting the activation of NF-κB signaling and binding to acetylated NF-κB p65 (lysine-310) in mouse macrophages.

scholarly journals Modulation of Macrophage Gene Expression via Liver X Receptor α Serine 198 Phosphorylation

2015 ◽  
Vol 35 (11) ◽  
pp. 2024-2034 ◽  
Author(s):  
Chaowei Wu ◽  
Maryem A. Hussein ◽  
Elina Shrestha ◽  
Sarah Leone ◽  
Mohammed S. Aiyegbo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Conformational Changes ◽  
Liver X Receptor ◽  
Raw264.7 Cells ◽  
Atherosclerotic Plaques ◽  
Ccr7 Expression ◽  
Mouse Macrophages ◽  
Liver X Receptor Α ◽  
Low Levels ◽  
Human And Mouse

In mouse models of atherosclerosis, normalization of hyperlipidemia promotes macrophage emigration and regression of atherosclerotic plaques in part by liver X receptor (LXR)-mediated induction of the chemokine receptor CCR7. Here we report that LXRα serine 198 (S198) phosphorylation modulates CCR7 expression. Low levels of S198 phosphorylation are observed in plaque macrophages in the regression environment where high levels of CCR7 expression are observed. Consistent with these findings, CCR7 gene expression in human and mouse macrophages cell lines is induced when LXRα at S198 is nonphosphorylated. In bone marrow-derived macrophages (BMDMs), we also observed induction of CCR7 by ligands that promote nonphosphorylated LXRα S198, and this was lost in LXR-deficient BMDMs. LXRα occupancy at the CCR7 promoter is enhanced and histone modifications associated with gene repression are reduced in RAW264.7 cells expressing nonphosphorylated LXRα (RAW-LXRα S198A) compared to RAW264.7 cells expressing wild-type (WT) phosphorylated LXRα (RAW-LXRα WT). Expression profiling of ligand-treated RAW-LXRα S198A cells compared to RAW-LXRα WT cells revealed induction of cell migratory and anti-inflammatory genes and repression of proinflammatory genes. Modeling of LXRα S198 in the nonphosphorylated and phosphorylated states identified phosphorylation-dependent conformational changes in the hinge region commensurate with the presence of sites for protein interaction. Therefore, gene transcription is regulated by LXRα S198 phosphorylation, including that of antiatherogenic genes such as CCR7.

scholarly journals Regulation of Lipopolysaccharide-Induced Interleukin-12 Production by Activation of Repressor Element GA-12 through Hyperactivation of the ERK Pathway

2006 ◽  
Vol 13 (8) ◽  
pp. 876-883 ◽  
Author(s):  
Shinji Saito ◽  
Motohiro Matsuura ◽  
Yoshikazu Hirai
Keyword(s):  
Peritoneal Macrophages ◽  
Raw264.7 Cells ◽  
Interleukin 12 ◽  
High Dose ◽  
Erk Pathway ◽  
Innate And Adaptive Immunity ◽  
Erk Activation ◽  
Extracellular Signal ◽  
Mouse Macrophages ◽  
Repressor Element

ABSTRACT Interleukin-12 (IL-12) functions as a representative lipopolysaccharide (LPS) mediator in both innate and adaptive immunity. We investigated the regulation of LPS-induced IL-12 production by mouse macrophages. In response to LPS, peritoneal macrophages produced bioactive IL-12 p70, a heterodimer (p40/p35) of subunits, but macrophage lines such as J774.1 and RAW264.7 did not. Induction of the p35 subunit was impaired in both cell lines, and additional impairment of p40 induction was observed in RAW264.7 cells. These results suggest that some negative regulatory mechanisms against LPS-induced IL-12 p40 production are constitutively functioning in RAW264.7 cells but not in the other types of cells. Activation of GA-12 (a repressor element of IL-12 p40), rather than suppression of promoter elements, such as binding sites for NF-κB, AP-1, and IRF-1, was detected in LPS-stimulated RAW264.7 cells, accompanying hyperactivation of extracellular signal-related kinase (ERK). When ERK activation was suppressed by an inhibitor (U0126), production of p40 rose from an undetectable to a substantial level and GA-12 activation decreased. In peritoneal macrophages, stimulation with a high dose of LPS reduced p40 production with enhanced activation of ERK. Pretreatment of the cells with phorbol myristate acetate to enhance ERK activation reduced p40 production in response to the optimal LPS stimulation. Taken together, these results demonstrate that hyperactivation of the ERK pathway plays a role in upstream signaling for the activation of GA-12, leading to the repression of IL-12 p40 production in mouse macrophages.

Metaxalone Suppresses Production of Inflammatory Cytokines Associated with Painful Conditions in Mouse Macrophages RAW264.7 Cells in Vitro: Synergistic Effect with β-caryophyllene

2020 ◽  
Vol 20 (8) ◽  
pp. 643-652
Author(s):  
Masayoshi Yamaguchi ◽  
Robert M. Levy
Keyword(s):  
Inflammatory Cytokines ◽  
Inhibitory Effect ◽  
Cell Number ◽  
Raw264.7 Cells ◽  
Mouse Macrophages ◽  
Fetal Bovine ◽  
Factor Α ◽  
Inflammatory Macrophages ◽  
Lps Treatment

Backgrounds and Objective: Inflammation is implicated in the pathogenesis of many diseases. Inflammatory cytokines with painful conditions are well known as biomarkers in human muscle pain, and they are produced by macrophages. Metaxalone is used as a skeletal muscle relaxant, but the mechanism by which metaxalone acts is unknown. This study was undertaken to investigate whether or not metaxalone exhibits an inhibitory effect on the activity of inflammatory macrophages in vitro. Methods: Mouse macrophage RAW264.7 cells were cultured in Dulbecco’s Modification of Eagle’s Medium containing 10% fetal bovine serum in the presence of metaxalone. Cell growth was assayed by counting the number of cells attached to culture dishes. Inflammatory cytokines released into the culture medium were analyzed with the ELISA kit. Results: Metaxalone (1-100 μM) was found to decrease the number of macrophages by inhibiting the proliferation and stimulating the death of RAW264.7 cells in vitro. The combination of metaxalone (0.1 or 1 μM) and β-caryophyllene (10 or 50 μM), which alone did not have a significant effect on the cell number, caused potential effects on the growth and death of RAW264.7 cells. Mechanistically, molecular levels of mitogenactivated protein kinase were decreased by treatment with metaxalone or β- caryophyllene, and each effect was enhanced by their combination. Furthermore, levels of caspase-3 were increased by metaxalone or β-caryophyllene and enhanced by their combination. Notably, productions of inflammatory cytokines, including tumor necrosis factor-α, interleukin-6 or prostaglandin E2, which were enhanced by lipopolysaccharide (LPS), were repressed by culturing with metaxalone. Levels of cyclooxygenase (COX)-1, COX-2 and nuclear factor kappa B, which were increased by LPS treatment, were reduced by metaxalone. Conclusion: Metaxalone was found to suppress the activity of inflammatory macrophages in vitro.

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