Ikarisoside A inhibits inducible nitric oxide synthase in lipopolysaccharide-stimulated RAW 264.7 cells via p38 kinase and nuclear factor-κB signaling pathways

Choi, Hee Joung; Eun, Jae-Soon; Park, Young-Ran; Kim, Dae Keun; Li, Rihua; Moon, Woo Sung; Park, Jeong Mi; Kim, Hyung Sup; Cho, Nam-Pyo; Cho, Sung‐Dae; Soh, Yunjo

doi:10.1016/j.ejphar.2008.09.032

Cited by 64 publications

(44 citation statements)

References 44 publications

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“…Moreover, some studies indicate that the NF-κB transcription factor plays an important part in the regulation of genes encoding the proinflammatory cytokines, adhesion molecules, chemokines, growth factors, and inflammation-associated enzymes. 9,[57][58][59][60] The present molecular modeling study suggests that the suppressive effects of Ti/TiO 2 on RAW 264.7 activation depend on two signaling pathways that are closely involved in the inflammatory processes ( Figure 6). Specifically, it was demonstrated that such nanotubular surfaces lead to the attenuation of macrophage inflammatory responses through the simultaneous inactivation of the p38/ERK/JNK MAPK and NF-κB pathways.…”

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confidence: 80%

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-κB pathways

Neacsu¹,

Mazare²,

Schmuki³

et al. 2015

IJN

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Biomaterial implantation in a living tissue triggers the activation of macrophages in inflammatory events, promoting the transcription of pro-inflammatory mediator genes. The initiation of macrophage inflammatory processes is mainly regulated by signaling proteins of mitogen-activated protein kinase (MAPK) and by nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways. We have previously shown that titania nanotubes modified Ti surfaces (Ti/TiO 2 ) mitigate the immune response, compared with flat Ti surfaces; however, little is known regarding the underlying mechanism. Therefore, the aim of this study is to investigate the mechanism(s) by which this nanotopography attenuates the inflammatory activity of macrophages. Thus, we analyzed the effects of TiO 2 nanotubes on the activation of MAPK and NF-κB signaling pathways in standard and lipopolysaccharide-evoked conditions. Results showed that the Ti/TiO 2 significantly reduce the expression levels of the phosphorylated forms of p38, ERK1/2, c-Jun NH 2 -terminal kinase (JNK), IKKβ, and IkB-α. Furthermore, a significant reduction in the p65 nuclear accumulation on the nanotubular surface was remarked. Following, by using specific MAPK inhibitors, we observed that lipopolysaccharide-induced production of monocyte chemotactic protein-1 and nitric oxide was significantly inhibited on the Ti/TiO 2 surface via p38 and ERK1/2, but not via JNK. However, the selective inhibitor for JNK signaling pathway (SP600125) was effective in reducing tumor necrosis factor alpha release as well as monocyte chemotactic protein-1 and nitric oxide production. Altogether, these data suggest that titania nanotubes can attenuate the macrophage inflammatory response via suppression of MAPK and NF-κB pathways providing a potential mechanism for their anti-inflammatory activity.

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mentioning

confidence: 80%

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-κB pathways

Neacsu¹,

Mazare²,

Schmuki³

et al. 2015

IJN

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“…To determine the appropriate concentration of roxatidine, which has no effect on cell viability, cytotoxicity studies were performed at 24 h following treatment of cells with various concentrations of roxatidine. Viabilities were determined using colorimetric MTT assays, as described previously [Choi et al, 2008].…”

Section: Cell Culture and Sample Treatmentmentioning

confidence: 99%

“…NITRITE DETERMINATION RAW 264.7 cells were plated at 1 Â 10 5 cells/well in 24 well-plates and then pretreated with various concentrations (40, 80, and 120 mM) of roxatidine for 1 h. After 1 h, the cells were stimulated with LPS (1 mg/ml) for 24 h. Nitrite levels in culture media were determined using the Griess reaction assay and presumed to reflect NO levels [Choi et al, 2008]. Briefly, 100 ml of cell culture medium was mixed with 100 ml of Griess reagent [equal volumes of 1% (w/v) sulfanilamide in 5% (v/v) phosphoric acid and 0.1% (w/v) naphtylethylenediamine-HCl], incubated at room temperature for 10 min, and then the absorbance at 540 nm was measured in a microplate reader (Perkin Elmer Cetus, Foster City, CA).…”

Section: Cell Culture and Sample Treatmentmentioning

confidence: 99%

Roxatidine suppresses inflammatory responses via inhibition of NF-κB and p38 MAPK activation in LPS-induced RAW 264.7 macrophages

Cho

Shin

et al. 2011

J. Cell. Biochem.

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Roxatidine is a novel, specific, competitive H(2) -receptor antagonist that is used to treat gastric and duodenal ulcers, and which is known to suppress the growth of several tumors by reducing vascular endothelial growth factor (VEGF) expression. Nevertheless, it remains unclear whether roxatidine has anti-inflammatory effects. In this study, we the authors investigated the anti-inflammatory effect of roxatidine in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. It was found that roxatidine dose-dependently inhibited the productions of prostaglandin E(2) (PGE(2)), nitric oxide (NO), and histamine, and the protein and mRNA expressions of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and histidine decarboxylase (HDC). In addition, roxatidine reduced the productions and expressions of VEGF-1 and pro-inflammatory cytokines, including those of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Electrophoretic mobility shift assays (EMSA) and reporter gene assays revealed that treatment with roxatidine attenuated the LPS-induced DNA-binding and transcriptional activity of nuclear factor kappa B (NF-κB). In addition, it was found that pretreatment with roxatidine significantly inhibited the nuclear translocations of the p65 and p50 subunits of NF-κB, and these inhibitions were not found to be associated with decreases in the phosphorylation or degradation of inhibitory kappa B-α (IκBα). Furthermore, roxatidine suppressed the phosphorylation of p38 MAP kinase, but not of IκB kinase-α/β (IKKα/β), c-Jun NH(2) -terminal kinase (JNK), or extracellular signal-regulated kinase (ERK). Taken together, these results indicate that the anti-inflammatory properties of roxatidine in LPS-treated RAW 264.7 macrophages are mediated by the inhibition of NF-κB transcriptional activity and the p38 MAP kinase pathway.

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“…Therefore, NO production induced by LPS through iNOS can reflect the degree of inflammation, and a change in NO level through inhibition of iNOS enzyme activity or iNOS induction provides a means of assessing the effect of agents on the inflammatory process (Zhou et al, 2007;Choi et al, 2008;Kanwar et al, 2009;O'Connor and O'Brien, 2009;Murakami, 2009). Prostaglandins also play a major role as mediators of the inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of Jeju endemic seaweeds on the production of pro-inflammatory mediators in mouse macrophage cell line RAW 264.7

Yang

Moon

Kim

et al. 2010

J. Zhejiang Univ. Sci. B

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Seaweed has been used in traditional cosmetics and as a herbal medicine in treatments for cough, boils, goiters, stomach ailments, and urinary diseases, and for reducing the incidence of tumors, ulcers, and headaches. Despite the fact that seaweeds are frequently used in the practice of human health, little is known about the role of seaweed in the context of inflammation. This study aimed to investigate the influence of Jeju endemic seaweed on a mouse macrophage cell line (RAW 264.7) under the stimulation of lipopolysaccharide (LPS). Ethyl acetate extracts obtained from 14 different kinds of Jeju seaweeds were screened for inhibitory effects on pro-inflammatory mediators. Our results revealed that extracts from five seaweeds, Laurencia okamurae, Grateloupia elliptica, Sargassum thunbergii, Gloiopeltis furcata, and Hizikia fusiformis, were potent inhibitors of the production of pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E 2 (PGE 2 ), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). Based on these results, the anti-inflammatory effects and low cell toxicity of these seaweed extracts suggest potential therapeutic applications in the regulation of the inflammatory response.

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Ikarisoside A inhibits inducible nitric oxide synthase in lipopolysaccharide-stimulated RAW 264.7 cells via p38 kinase and nuclear factor-κB signaling pathways

Cited by 64 publications

References 44 publications

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-κB pathways

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-κB pathways

Roxatidine suppresses inflammatory responses via inhibition of NF-κB and p38 MAPK activation in LPS-induced RAW 264.7 macrophages

Inhibitory effect of Jeju endemic seaweeds on the production of pro-inflammatory mediators in mouse macrophage cell line RAW 264.7

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Ikarisoside A inhibits inducible nitric oxide synthase in lipopolysaccharide-stimulated RAW 264.7 cells via p38 kinase and nuclear factor-κB signaling pathways

Cited by 64 publications

References 44 publications

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-&kappa;B pathways

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-&kappa;B pathways

Roxatidine suppresses inflammatory responses via inhibition of NF-κB and p38 MAPK activation in LPS-induced RAW 264.7 macrophages

Inhibitory effect of Jeju endemic seaweeds on the production of pro-inflammatory mediators in mouse macrophage cell line RAW 264.7

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Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-κB pathways

Attenuation of the macrophage inflammatory activity by TiO2 nanotubes via inhibition of MAPK and NF-κB pathways