Inhibitory effects of a spinasterol glycoside on lipopolysaccharide-induced production of nitric oxide and proinflammatory cytokines via down-regulating MAP kinase pathways and NF-κB activation in RAW264.7 macrophage cells

Lee, Tae Hoon; Jung, Mira; Bang, Myun‐Ho; Chung, Dae Kyun; Kim, Jiyoung

doi:10.1016/j.intimp.2012.05.005

Cited by 42 publications

(32 citation statements)

References 39 publications

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“…NO is an important inflammatory mediator produced by macrophages and other cells in response to bacterial products like LPS (47)(48)(49). In RAW 264.7 cells, NO is enzymatically produced in the presence of inflammatory stimuli through the induction of iNOS (45,50). We next determined whether DMA affects expression of LPS-induced iNOS and, as expected, and in agreement with its effect on NO secretion, iNOS expression was reduced by 10 mM DMA.…”

Section: Dma Inhibits the Transcriptional Activity Of Nf-κb But Not Asupporting

confidence: 61%

“…In the present work, we first determined the effect of DMA on NO −2 secretion as an initial evaluation of its antiinflammatory potential in LPS-stimulated RAW 264.7 cells (43)(44)(45). Our data reveal that DMA at 10 mM results in a 21% reduction in NO −2 levels in LPS-induced RAW 264.7 cells, as compared with the LPS control.…”

Section: Dma Inhibits the Transcriptional Activity Of Nf-κb But Not Amentioning

confidence: 91%

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N,N-Dimethylacetamide Significantly Attenuates LPS- and TNFα-Induced Proinflammatory Responses Via Inhibition of the Nuclear Factor Kappa B Pathway

Pekson

Poltoratsky

Gorasiya

et al. 2016

Mol Med

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Previously, we have shown that N,N-dimethylacetamide (DMA) prevents inflammation-induced preterm birth in a murine model, inhibits lipopolysaccharide (LPS)-induced increases in placental proinflammatory cytokines and upregulates the antiinflammatory cytokine interleukin-10 (IL-10). However, DMA's mechanism of action remains to be elucidated. In the current study, we investigate how DMA produces its antiinflammatory effect. Using in vitro and ex vivo models, we show that DMA suppresses secretion of proinflammatory cytokines in lipopolysaccharide (LPS)-induced RAW 264.7 cells, TNFα-challenged JEG-3 cells and LPS-stimulated human placental explants. DMA significantly attenuated secretion of TNFα, IL-6, IL-10 and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells; IL-6 secretion from TNFα-stimulated JEG-3 cells; and TNFα, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. We further investigated whether DMA's effect on cytokine expression involves the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. DMA (10 mM) significantly inhibited degradation of nuclear factor of kappa light polypeptide gene enhancer in B cell inhibitor α (IκBα) in LPS-stimulated RAW 264.7 cells, but there was no significant change in the expression of phosphorylated or native forms of downstream proteins in the MAPK pathway. In addition, DMA significantly attenuated luciferase activity in cells co-transfected with NF-κB-Luc reporter plasmid, but not with AP-1-Luc or CEBP-Luc reporters. Overall, our findings suggest that the antiinflammatory activity of DMA is mediated by inhibition of the NF-κB pathway via decreased IκBα degradation.

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Section: Dma Inhibits the Transcriptional Activity Of Nf-κb But Not Asupporting

confidence: 61%

Section: Dma Inhibits the Transcriptional Activity Of Nf-κb But Not Amentioning

confidence: 91%

N,N-Dimethylacetamide Significantly Attenuates LPS- and TNFα-Induced Proinflammatory Responses Via Inhibition of the Nuclear Factor Kappa B Pathway

Pekson

Poltoratsky

Gorasiya

et al. 2016

Mol Med

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“…15 The amount of NO was determined by measuring the absorbance at 550 nm. The cell viability was determined by the 3-[4,5-dimetnythiazol-2-yl]-2,5-diphenyl-thetazolium bromide (MTT)-based colorimetric assay as previously described.…”

Section: Materials and Cell Culturementioning

confidence: 99%

“…The cell viability was determined by the 3-[4,5-dimetnythiazol-2-yl]-2,5-diphenyl-thetazolium bromide (MTT)-based colorimetric assay as previously described. 15 Reverse transcriptase-polymerase chain reaction analysis…”

Section: Materials and Cell Culturementioning

confidence: 99%

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Cynandione A attenuates lipopolysaccharide-induced production of inflammatory mediators via MAPK inhibition and NF-κB inactivation in RAW264.7 macrophages and protects mice against endotoxin shock

Kim

Lee

et al. 2014

Exp Biol Med (Maywood)

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Cynanchum wilfordii has been traditionally used in eastern Asia for the treatment of various diseases such as gastrointestinal diseases and arteriosclerosis. Cynandione A (CA), an acetophenone, is one of major constituents from roots of C. wilfordii. In the present study, the anti-inflammatory activities of CA were investigated in lipopolysaccharide (LPS)-treated RAW264.7 macrophages and LPS-administered C57BL/6 N mice. CA significantly decreased LPS-induced production of nitric oxide and prostaglandin E 2 in a dose-dependent manner, while CA up to 200 mM did not exhibit cytotoxic activity. Our data also showed that CA significantly attenuated expression of iNOS and COX-2 in LPS-stimulated macrophages. CA inhibited phosphorylation of IkB-a and MAP kinases such as ERK and p38. Furthermore, we demonstrated that CA inhibited translocation of NF-kB to the nucleus, transcription of the NF-kB minimal promoter and NF-kB DNA binding activity. Administration of CA significantly decreased the plasma levels of pro-inflammatory cytokines such as TNF-a, IL-6, and IL-1b in LPS-injected mice and improved survival of septic mice with lethal endotoxemia. These results demonstrate that CA has effective inhibitory effects on production of inflammatory mediators via suppressing activation of NF-kB and MAPK signaling pathways, suggesting that CA may be used as a potential antiinflammatory agent for the prevention and treatment of inflammatory diseases.

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Phytosterols

Zhu¹,

Nyström²

2019

Whole Grains and Their Bioactives

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Inhibitory effects of a spinasterol glycoside on lipopolysaccharide-induced production of nitric oxide and proinflammatory cytokines via down-regulating MAP kinase pathways and NF-κB activation in RAW264.7 macrophage cells

Cited by 42 publications

References 39 publications

N,N-Dimethylacetamide Significantly Attenuates LPS- and TNFα-Induced Proinflammatory Responses Via Inhibition of the Nuclear Factor Kappa B Pathway

N,N-Dimethylacetamide Significantly Attenuates LPS- and TNFα-Induced Proinflammatory Responses Via Inhibition of the Nuclear Factor Kappa B Pathway

Cynandione A attenuates lipopolysaccharide-induced production of inflammatory mediators via MAPK inhibition and NF-κB inactivation in RAW264.7 macrophages and protects mice against endotoxin shock

Phytosterols

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