Coccomyxa Gloeobotrydiformis Polysaccharide Inhibits Lipopolysaccharide-Induced Inflammation in RAW 264.7 Macrophages

Dai, Bo; Wei, Dan; Zheng, Ningning; Chen, Zhihong; Xin, Na; Ma, Tiantian; Zheng, Lan; Sumi, Ryo; Sun, Liang

doi:10.1159/000495922

Cited by 52 publications

(28 citation statements)

References 39 publications

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“…Pretreatment with Ls-ME suppressed the reduction in cell viability ( Figure 1 C). With respect to the morphology of activated macrophages, the LPS-treated group demonstrated an altered shape in comparison with the untreated group [ 22 ]. The cells retained original round shape in the group that was subjected to pretreatment with Ls-ME despite stimulation with LPS ( Figure 1 D).…”

Section: Resultsmentioning

confidence: 99%

“…Since NO and ROS are well-known pro-inflammatory mediators that play an essential role in the inflammatory process, the effects of Ls-ME on LPS-induced inflammatory response in RAW 264.7 cells were investigated by the detection NO levels and intracellular ROS production [22,23]. The generation of NO was remarkably enhanced in response to the stimulation with LPS.…”

Section: Ls-me Reduces No Ros and Tnf-α Productionmentioning

confidence: 99%

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Effects of Launaea sarmentosa Extract on Lipopolysaccharide-Induced Inflammation via Suppression of NF-κB/MAPK Signaling and Nrf2 Activation

et al. 2020

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Launaea sarmentosa has been extensively used as a nutrient herb in traditional Vietnamese remedies for the treatment of various diseases, especially inflammatory diseases. However, no detailed research has been conducted examining the molecular mechanisms involved in the suppression of inflammatory response. Here, we studied the effects of L. sarmentosa methanol extract on lipopolysaccharide (LPS)-induced inflammation using RAW 264.7 macrophages. The extract demonstrated potent antioxidant activity owing to the presence of polyphenolic and flavonoid components. Pretreatment with the extract inhibited LPS-mediated secretion of nitric oxide, reactive oxygen species, and tumor necrosis factor-α as well as the expression of inflammatory cytokines. Furthermore, the activation of the nuclear factor-kappa B pathway and phosphoinositide-3-kinase/protein kinase B pathways was blocked by the extract by inhibiting Akt phosphorylation. Additionally, the mitogen-activated protein kinase pathway was suppressed, and endoplasmic reticulum stress was attenuated. Furthermore, the extract promoted the activity of nuclear factor erythroid-2-related factor 2 resulting in the up-regulation of heme oxygenase-1 pathway, leading to the suppression of oxidative stress and inflammatory response. Taken together, the results indicate that L. sarmentosa exhibits anti-inflammatory effects, and hence, can be further developed as a novel drug for the treatment of diseases associated with excessive inflammation.

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Section: Resultsmentioning

confidence: 99%

Section: Ls-me Reduces No Ros and Tnf-α Productionmentioning

confidence: 99%

Effects of Launaea sarmentosa Extract on Lipopolysaccharide-Induced Inflammation via Suppression of NF-κB/MAPK Signaling and Nrf2 Activation

et al. 2020

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“…Immunofluorescence assay was applied to detect the expression with confocal spectral microscopy, as described previously 22 . RAW 264.7 cells were seeded onto glass coverslips overnight and treated with PIPO for 1 hour before incubating with LPS.…”

Section: Methodsmentioning

confidence: 99%

“…Immunofluorescence assay was applied to detect the expression with confocal spectral microscopy, as described previously. 22 RAW 264.7 cells were seeded onto glass coverslips overnight and treated with PIPO for 1 hour before incubating with LPS. After exposure, cells were treated with cold 4% paraformaldehyde for 20 minutes and permeabilized using 0.5% Triton-X 100 for 30 minutes.…”

Section: Immunofluorescence Assaymentioning

confidence: 99%

Pipoxolan suppresses the inflammatory factors of NF‐κB, AP‐1, and STATs, but activates the antioxidative factor Nrf2 in LPS‐stimulated RAW 264.7 murine macrophage cells

Lin

Chang

et al. 2020

Environmental Toxicology

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Although pipoxolan (PIPO) is a smooth muscle relaxant, its anti‐inflammatory capability has not been studied. Therefore, we investigated the anti‐inflammatory molecular mechanisms of PIPO in lipopolysaccharide (LPS)‐induced RAW 264.7 macrophages. In this study, we used the MTT assay to evaluate the cytotoxicity, applied the enzyme‐linked immunosorbent assay to determine the inflammatory cytokines, and performed Western blotting to assess protein expression. The results showed that PIPO significantly inhibited cytokine production, including nitric oxide, prostaglandin E2, tumor necrosis factor‐α, and interleukin‐6. PIPO also suppressed the pro‐inflammatory mediator expression with inducible nitric oxide synthase and cyclooxygenase‐2. Moreover, PIPO prohibited the multiple inflammatory transcription factor pathways, including inhibitor kappa B/nuclear factor of the κ light chain enhancer of B cells (NF‐κB), mitogen‐activated protein kinase/activator protein‐1 (AP‐1), Janus kinase/signal transducer and activator of transcription (STAT), and toll‐like receptor 4 (TLR4)/serine/threonine kinase (AKT). Besides, PIPO effectively activated the nuclear factor erythroid 2‐related factor 2 (Nrf2)/heme oxygenase‐1 antioxidative pathway. Collectively, PIPO may attenuate the inflammatory effects via influencing the LPS/TLR4 receptor binding; suppress the expression of anti‐inflammatory transcription factors NF‐κB, AP‐1, and STAT; and activating the antioxidative transcription factor Nrf2 in LPS‐stimulated mouse RAW 264.7 cells.

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“…NF-κB transactivation is crucial for the upregulation of various pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) [ 10 ]. It has been reported that the Janus kinases-signal transducer and activator of transcription (JAK-STAT) protein signaling pathway is associated with increased pro-inflammatory mediators, such as inducible-nitric oxide synthase (iNOS), that produce nitric oxide (NO) [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Minor Ginsenoside Rg2 and Rh1 Attenuates LPS-Induced Acute Liver and Kidney Damages via Downregulating Activation of TLR4-STAT1 and Inflammatory Cytokine Production in Macrophages

Huynh

Baek

Sim

et al. 2020

IJMS

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Ginsenosides have been reported to have various biological effects, such as immune regulation and anticancer activity. In this study, we investigated the anti-inflammatory role of a combination of Rg2 and Rh1, which are minor ginsenosides, in lipopolysaccharide (LPS)-stimulated inflammation. In vitro experiments were performed using the RAW264.7 cell line, and an in vivo model of inflammation was established using LPS-treated ICR mice. We employed Griess assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, quantitative reverse transcriptase-polymerase chain reaction, western blotting, immunofluorescence staining, and hematoxylin and eosin staining to evaluate the effect of Rg2 and Rh1. We found that Rg2 and Rh1 significantly decreased LPS-induced major inflammatory mediator production, inducible-nitric oxide synthase expression, and nitric oxide production in macrophages. Moreover, Rg2 and Rh1 combination treatment inhibited the binding of LPS to toll-like receptor 4 (TLR4) on peritoneal macrophages. Therefore, the combination of ginsenoside Rg2 and Rh1 suppressed inflammation by abolishing the binding of LPS to TLR4, thereby inhibiting the TLR4-mediated signaling pathway. The combined ginsenoside synergistically blocked LPS-mediated PKCδ translocation to the plasma membrane, resulting in p38-STAT1 activation and NF-κB translocation. In addition, mRNA levels of pro-inflammatory cytokines, including TNF-α, IL-1β, and IFN-β, were significantly decreased by combined ginsenoside treatment. Notably, the 20 mg/kg ginsenoside treatment significantly reduced LPS-induced acute tissue inflammation levels in vivo, as indicated by the tissue histological damage scores and the levels of biochemical markers for liver and kidney function from mouse serum. These results suggest that the minor ginsenosides Rg2 and Rh1 may play a key role in prevention of LPS-induced acute inflammation and tissue damage.

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Coccomyxa Gloeobotrydiformis Polysaccharide Inhibits Lipopolysaccharide-Induced Inflammation in RAW 264.7 Macrophages

Cited by 52 publications

References 39 publications

Effects of Launaea sarmentosa Extract on Lipopolysaccharide-Induced Inflammation via Suppression of NF-κB/MAPK Signaling and Nrf2 Activation

Effects of Launaea sarmentosa Extract on Lipopolysaccharide-Induced Inflammation via Suppression of NF-κB/MAPK Signaling and Nrf2 Activation

Pipoxolan suppresses the inflammatory factors of NF‐κB, AP‐1, and STATs, but activates the antioxidative factor Nrf2 in LPS‐stimulated RAW 264.7 murine macrophage cells

Minor Ginsenoside Rg2 and Rh1 Attenuates LPS-Induced Acute Liver and Kidney Damages via Downregulating Activation of TLR4-STAT1 and Inflammatory Cytokine Production in Macrophages

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