A phenolic acid phenethyl urea compound inhibits lipopolysaccharide-induced production of nitric oxide and pro-inflammatory cytokines in cell culture

Hwang, Jeong Hwan; Yu, Ji‐Yeon; Jang, Young-Oh; Kim, Beom‐Tae; Hwang, Kyung Ho; Jeon, Young-Mi; Lee, Jeong-Chae

doi:10.1016/j.intimp.2010.01.016

Cited by 14 publications

(11 citation statements)

References 35 publications

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“…Recently, inhibitors of the phosphorylation of JNK, but not of ERK, were reported to reduce LPS-stimulated NO production (Lin et al, 2009). In contrast, Hwang et al (2010) reported that the inhibitors of phosphorylation of ERK and p-38, but not of JNK, reduced LPS-stimulated NO production. In the present study, a MAPK-ERK kinase 1 (MEK1) inhibitor (PD98059) acting on the phosphorylation of ERK and an ERK inhibitor (FR180204) showed less inhibition against the production of NO; −2.4 ± 1.1% inhibition at 100 M and 7.2 ± 2.2% inhibition at 10 M, respectively.…”

Section: Resultsmentioning

confidence: 99%

Suppressive effects of methoxyflavonoids isolated from Kaempferia parviflora on inducible nitric oxide synthase (iNOS) expression in RAW 264.7 cells

Sae-Wong

Matsuda

Tewtrakul

et al. 2011

Journal of Ethnopharmacology

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Section: Resultsmentioning

confidence: 99%

Suppressive effects of methoxyflavonoids isolated from Kaempferia parviflora on inducible nitric oxide synthase (iNOS) expression in RAW 264.7 cells

Sae-Wong

Matsuda

Tewtrakul

et al. 2011

Journal of Ethnopharmacology

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“…This study demonstrated the ability of acteoside to reduce production of inflammatory cytokines such as TNF-α, IL-1β, and IL-6 in macrophages. Acteoside is thought to inhibit inflammatory cytokine production by suppressing p38 kinase and ERK signaling, because activating ERK1/2, p38 MAPK, or both is required for lipopolysaccharide-induced production of these cytokines in macrophages [40], [41]. Luteolin, an inflammatory compound, had also been reported to suppress the production of inflammatory mediators by inhibiting p38 MAPK activation [42].…”

Section: Discussionmentioning

confidence: 99%

Acteoside Suppresses RANKL-Mediated Osteoclastogenesis by Inhibiting c-Fos Induction and NF-κB Pathway and Attenuating ROS Production

Lee

et al. 2013

PLoS ONE

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Numerous studies have reported that inflammatory cytokines are important mediators for osteoclastogenesis, thereby causing excessive bone resorption and osteoporosis. Acteoside, the main active compound of Rehmannia glutinosa, which is used widely in traditional Oriental medicine, has anti-inflammatory and antioxidant potentials. In this study, we found that acteoside markedly inhibited osteoclast differentiation and formation from bone marrow macrophages (BMMs) and RAW264.7 macrophages stimulated by the receptor activator of nuclear factor-kappaB (NF-κB) ligand (RANKL). Acteoside pretreatment also prevented bone resorption by mature osteoclasts in a dose-dependent manner. Acteoside (10 µM) attenuated RANKL-stimulated activation of p38 kinase, extracellular signal-regulated kinases, and c-Jun N-terminal kinase, and also suppressed NF-κB activation by inhibiting phosphorylation of the p65 subunit and the inhibitor κBα. In addition, RANKL-mediated increases in the expression of c-Fos and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) and in the production of tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 were apparently inhibited by acteoside pretreatment. Further, oral acteoside reduced ovariectomy-induced bone loss and inflammatory cytokine production to control levels. Our data suggest that acteoside inhibits osteoclast differentiation and maturation from osteoclastic precursors by suppressing RANKL-induced activation of mitogen-activated protein kinases and transcription factors such as NF-κB, c-Fos, and NFATc1. Collectively, these results suggest that acteoside may act as an anti-resorptive agent to reduce bone loss by blocking osteoclast activation.

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“…We found that LPS stimulation at 100 ng/ml for 19 h can trigger NOP. This treatment is less aggressive than other treatments used previously; 1 μg/ml ( 34 – 37 , 47 ) and 10 μg/ml ( 25 , 48 ) . Also, this concentration is useful for testing whether polyphenols can exert an inhibitory effect, as seen in previous studies of inflammation ( 17 ) .…”

Section: Discussionmentioning

confidence: 77%

“…The phosphorylated proteins, P-NF-κB p65, P-SAPK/JNK, P-p38, P-IκB-α and P-STAT3, were tested. RAW 264.7 macrophages were stimulated with LPS (100 ng/ml) for 30 min to detect phosphoprotein levels in these conditions ( 33 – 37 ) . At the same time, different concentrations of the following compounds were applied to different groups of cells: Res (2·5 μg/ml), EPA (30 μ m ) and Res+EPA (2·5 μg/ml, 30 μ m ).…”

Section: Resultsmentioning

confidence: 99%

Enhanced anti-inflammatory effect of resveratrol and EPA in treated endotoxin-activated RAW 264.7 macrophages

et al. 2012

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Macrophages play an important role in immunogenic challenges by producing reactive oxygen species, NO and proinflammatory cytokines that can aggravate and propagate local inflammation. Multiple mechanisms regulate these inflammatory processes. NF-kB and activator protein 1 pathways are crucial in the expression of proinflammatory genes, such as TNF-a, IL-1 (a or b) and -6. Some polyphenols, which are present in beverages, vegetables and fruits, and PUFA, which are present in marine oils and fish food, possess anti-inflammatory effects in vivo and in vitro. Our aim in the present study was to assess whether polyphenols and PUFA have synergistic anti-inflammatory effects in murine macrophages in vitro. Inflammation in RAW 264.7 macrophages was induced by lipopolysaccharide at 100 ng/ml. The treatments with molecules were performed by co-incubation for 19 h. A NO production assay by Griess reaction, a phosphoprotein assay by Pathscan ELISA kit and gene expression analysis using the TaqMan w Low-density Array for ninety-one genes related to inflammation, oxidative stress and metabolism were performed to assess the synergistic anti-inflammatory effects of polyphenols, epigallocatechin gallate and resveratrol (Res; 2·5 mg/ml), and the PUFA, DHA and EPA (30 mM). Adding Res þ EPA had an enhanced anti-inflammatory effect, in comparison with EPA and Res alone, leading to decreased NO levels; modulating the phospho-stress activated protein kinase/Jun N-terminal kinase (P-SAPK/JNK) level; down-regulating proinflammatory genes, such as IL, chemokines, transcription factors; and up-regulating several antioxidant genes. Therefore, this combination has a stronger anti-inflammatory effect than either of these molecules separately in RAW macrophages.

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A phenolic acid phenethyl urea compound inhibits lipopolysaccharide-induced production of nitric oxide and pro-inflammatory cytokines in cell culture

Cited by 14 publications

References 35 publications

Suppressive effects of methoxyflavonoids isolated from Kaempferia parviflora on inducible nitric oxide synthase (iNOS) expression in RAW 264.7 cells

Suppressive effects of methoxyflavonoids isolated from Kaempferia parviflora on inducible nitric oxide synthase (iNOS) expression in RAW 264.7 cells

Acteoside Suppresses RANKL-Mediated Osteoclastogenesis by Inhibiting c-Fos Induction and NF-κB Pathway and Attenuating ROS Production

Enhanced anti-inflammatory effect of resveratrol and EPA in treated endotoxin-activated RAW 264.7 macrophages

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