• Fisheries and Aquatic Sciences
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• v.21 no.5
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• pp.14.1-14.8
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• 2018

The objective of this study was to investigate the anti-inflammatory effects of the pepsinolytic hydrolysate from the fish frame, Johnius belengerii, on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. The J. belengerii frame hydrolysate (JFH) significantly suppressed nitric oxide (NO) secretion on LPS-stimulated RAW264.7 macrophages. Moreover, the JFH markedly inhibited the levels of protein and mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Furthermore, the LPS-stimulated mRNA expression of pro-inflammatory cytokines, including tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 was downregulated when cells were cultured with the JFH. The JFH significantly reduced the phosphorylation of c-Jun N-terminal kinase (JNK) and the translocation of nuclear factor-kappa B ($NF-{\kappa}B$) in macrophages. As the result, the JFH has the potential anti-inflammatory activity via blocking the JNK and $NF-{\kappa}B$ signal pathways.

• The Korea Journal of Herbology
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• v.34 no.1
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• pp.91-98
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• 2019

Objectives : While inducing inflammatory response due to LPS it will investigate mechanism associated with anti-inflammatory effects from macrophages and provide basic data for the possible use as anti-inflammatory materials. Methods : We investigated cell viability, NO, $TNF-{\alpha}$ and IL-6 by ELISA and expressions of iNOS, COX-2, MAPKs and $NF-{\kappa}B$ were measured in RAW 264.7 cells induced by LPS. Results : The cell viability of Parthenocissus tricuspidata extracts(PTE) identified in macrophages showed that cell viability rate was more than 99% at the concentration of 8, 40, and $200{\mu}g/mL$. NO generated amounts revealed that it relied on concentration and was significantly reduced compared to the control. The expression of iNOS was restrained by the control at the concentration of 200 and $400{\mu}g/mL$. In addition, the expression of COX-2 was found to be significantly reduced to the untreated control at the concentration of $400{\mu}g/mL$. $TNF-{\alpha}$ relied on concentration and showed a significant decreased compared to the control. In contrast, IL-6 relied on concentration, reduced compared to the control. Phosphorylation of ERK, JNK, and p38 mediated by LPS were restrained by relying on concentration. Phosphorylation and decomposition of $I{\kappa}B{\alpha}$ as well as p65 nuclear transmission of $NF-{\kappa}B$ subunit were restrained. Conclusions : By restraining the activation of $NF-{\kappa}B$, anti-inflammatory effects were revealed by reducing phosphorylative activation of MAPKs, restraining the expression of iNOS and COX-2 and restraining the creation of NO, IL-6, and $TNF-{\alpha}$. Therefore, it can be assumed that they can be used as a variety of anti-inflammatory materials.

• Fisheries and Aquatic Sciences
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• v.17 no.1
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• pp.27-35
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• 2014

Marine brown algae have been identified as a rich source of structurally diverse bioactive compounds. Whether Myagropsis yendoi ethanolic extracts (MYE) inhibit inflammatory responses was investigated using lipopolysaccharide (LPS)-stimulated microglia BV-2 cells. MYE inhibited LPS-induced nitric oxide (NO) production in a dose-dependent manner and suppressed the expression of inducible nitric oxide synthase in BV-2 cells. MYE also reduced the production of pro-inflammatory cytokines in LPS-stimulated BV-2 cells. LPS-induced nuclear factor-${\kappa}B$ (NF-${\kappa}B$) transcriptional activity and NF-${\kappa}B$ translocation into the nucleus were significantly inhibited by MYE treatment through preventing degradation of the inhibitor ${\kappa}B-{\alpha}$. Moreover, MYE inhibited the phosphorylation of AKT, ERK, JNK, and p38 mitogen-activated protein kinase in LPS-stimulated BV-2 cells. These results indicate that MYE is a potential source of therapeutic or functional agents for neuroinflammatory diseases.

• BMB Reports
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• v.45 no.3
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• pp.177-182
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• 2012

Camellia japonica oil (CJ oil) has been used traditionally in East Asia to nourish and soothe the skin as well as help restore the elasticity of skin. CJ oil has also been used on all types of bleeding instances. However, little is known about its anti-inflammatory effects. Therefore, the anti-inflammatory effects of CJ oil and its mechanisms of action were investigated. CJ oil inhibited LPS-induced production of NO, $PGE_2$, and TNF-${\alpha}$ in RAW264.7 cells. In addition, expression of COX-2 and iNOS genes was reduced. To evaluate the mechanism of the anti-inflammatory activity of CJ oil, LPS-induced activation of AP-1 and NF-${\kappa}B$ promoters was found to be significantly reduced by CJ oil. LPS-induced phosphorylation of $I{\kappa}B{\alpha}$, ERK, p38, and JNK was also attenuated. Our results indicate that CJ oil exerts anti-inflammatory effects by downregulating the expression of iNOS and COX-2 genes through inhibition of NF-${\kappa}B$ and AP-1 signaling.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.21 no.3
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• pp.82-93
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• 2008

Objective: Previously, the methanol extracts of the semen of Xanthium strumsrium could involved anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated Raw 264,7 cells, We evaluated the anti-allergic effects of X. strumarium on rat basophilic leukemia (RBL-2H3) cells, Methodes : To investigate the effect of X. strumarium on the phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187-induced RBL-2H3 cells. The effects of X. strumarium on the degranulation and the pro-inflammatory cytokines secretion and expression from RBL-2H3 cells were evaluated with $\beta$-hexosaminidase assay, ELISA, and RT-PCR analysis, In addition, we examined the effects of X. strumarium on nuclear factor (NF)-${\kappa}B$ activation and $I{\kappa}B-\alpha$ degradation using Western blot analysis. Results : X. strumarium inhibited degranulation and secretions and expressions of pro-inflammatory cytokines, such as tumor necrosis factor-alpha ($TNF-\alpha$), interleukin (IL)-4 and cyclooxygenase (COX)-2, on stimulated RBL-2H3 cells, however, X. strumarium not affect cell viability. In stimulated RBL-2H3 cells, the protein expression level of nuclear factor-kappa B (NF-${\kappa}B$) was decreased in the nucleus by X. strumarium. In addition, X. strumarium suppressed the degradation of inhibitory protein $I{\kappa}B-{\alpha}$ protein in RBL-2H3 cells. Conclusion : These results suggest that X. strumarium inhibits the degranulation and secretion of pro-inflammatory cytokines through blockade of NF-${\kappa}B$ activation and I $I{\kappa}B-{\alpha}$ degradation.

• Korean Journal of Plant Resources
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• v.31 no.6
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• pp.634-640
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• 2018

Aralia cordata (A. cordata), which belongs to Araliaceae, is a perennial herb widely distributed in East Asia. We evaluated the anti-inflammatory effect of stems (AC-S), roots (AC-R) and leaves (AC-L) extracted with 100% methanol of A. cordata and elucidated the potential signaling pathway in LPS-stimulated RAW264.7 cells. The AC-L showed a strong anti-inflammatory activity through inhibition of NO production. AC-L dose-dependently inhibited NO production by suppressing iNOS, COX-2 and $IL-{\beta}$ expression in LPS-stimulated RAW264.7 cells. AC-L inhibited the degradation and phosphorylation of $I{\kappa}B-{\alpha}$, which donated to the inhibition of p65 nuclear accumulation and $NF-{\kappa}B$ activation. Furthermore, AC-L suppressed the phosphorylation of ERK1/2 and p38. These results suggested that AC-L may utilize anti-inflammatory activity by blocking $NF-{\kappa}B$ and MAPK signaling pathway and indicated that the AC-L can be used as a natural anti-inflammatory drugs.

• The Korean Journal of Food And Nutrition
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• v.28 no.4
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• pp.551-557
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• 2015

The genus Rosa (Rosaceae) is an abundant source of phenolics and is traditionally used as a food supplement and as herbal medicine. Various plant phenolics are known to have anticancer, antioxidant, and anti-inflammatory properties. In this study, we investigated the anti-inflammatory effects of rose methanolic extracts (RMEs) from four different rose cultivars (Macarena, Onnuri, Oklahoma, and Colorado) in lipopolysaccharide (LPS)-activated RAW 264.7 cells. Our results demonstrated that pretreatment of REMs ($500{\mu}g/mL$) significantly reduced NO production by suppressing iNOS protein expression in LPS-stimulated cells. Anti-inflammatory effects by RMEs were observed in the following order: Oklahoma > Colorado > Onnuri > Macarena. Consistent with this finding, RMEs inhibited the translocation of $NF-{\kappa}B$ from the cytosol to the nucleus via the suppression of $I{\kappa}B{\alpha}$ phosphorylation and also inhibited LPS-stimulated $NF-{\kappa}B$ transcriptional activity. These findings suggest that RMEs exert anti-inflammatory actions and help to elucidate the mechanisms underlying the potential therapeutic values of RMEs. Therefore, RMEs could be regarded as a potential source of natural anti-inflammatory agents.

• Korean Journal of Plant Resources
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• v.27 no.3
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• pp.209-214
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• 2014

In this study, we investigated whether A. distichum decreases the production of inflammatory mediators through downregulation of the NF-${\kappa}B$ and ERK pathway. Our data indicated that A. distichum leaf inhibits the overexpression of iNOS in protein and mRNA levels, and subsequently blocked LPS-mediated NO overproduction in RAW264.7 cells. A. distichum leaf inhibited $I{\kappa}B-{\alpha}$ degradation and p65 nuclear translocation, and subsequently suppressed transcriptional activity of NF-${\kappa}B$ in LPS-stimulated RAW264.7 cells. In addition, A. distichum leaf suppressed LPS-induced ERK1/2 activation by decreasing phosphorylation of ERK1/2. These findings suggest that A. distichum leaf shows anti-inflammatory activities through suppressing ERK-mediated NF-${\kappa}B$ activation in mouse macrophage.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.91-99
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• 2016

(E)-3-(3-methoxyphenyl)-1-(2-pyrrolyl)-2-propenone (MPP) is an aldol condensation product resulting from pyrrole-2-carbaldehyde and m- and p- substituted acetophenones. However, its biological activity has not yet been evaluated. Since it has been reported that some propenone-type compounds display anti-inflammatory activity, we investigated whether MPP could negatively modulate inflammatory responses. To do this, we employed lipopolysaccharide (LPS)-stimulated macrophage-like RAW264.7 cells and examined the inhibitory levels of nitric oxide (NO) production and transcriptional activation, as well as the target proteins involved in the inflammatory signaling cascade. Interestingly, MPP was found to reduce the production of NO in LPS-treated RAW264.7 cells, without causing cytotoxicity. Moreover, this compound suppressed the mRNA levels of inflammatory genes, such as inducible NO synthase (iNOS) and tumor necrosis factor (TNF)-${\alpha}$. Using luciferase reporter gene assays performed in HEK293 cells and immunoblotting analysis with nuclear protein fractions, we determined that MPP reduced the transcriptional activation of nuclear factor (NF)-${\kappa}B$. Furthermore, the activation of a series of upstream signals for NF-${\kappa}B$ activation, composed of Src, Syk, Akt, and $I{\kappa}B{\alpha}$, were also blocked by this compound. It was confirmed that MPP was able to suppress autophosphorylation of overexpressed Src and Syk in HEK293 cells. Therefore, these results suggest that MPP can function as an anti-inflammatory drug with NF-${\kappa}B$ inhibitory properties via the suppression of Src and Syk.

• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.3
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• pp.293-300
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• 2012

Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are important inflammatory mediators implicated in pathogenesis of inflammation and certain types of human cancers. The present study was designed to determine whether Red Ginseng (RG) could modulate $I{\kappa}B$-kinase, iNOS and COX-2 gene expression and immune responses in RAW 264.7 macrophages stimulated with lipopolysaccharide (LPS). RG extract suppressed the expression of LPS-induced $I{\kappa}B$, iNOS, COX-2, and immune responses in a dose-dependent manner. It also showed an anti-inflammatory effect by inhibiting NF-${\kappa}B$ immune response induced by LPS treatment. Inhibitory effect of RG on LPS-induced inflammation was mediated by suppressed phosphorylation of ERK, JNK and p38 through the regulation of the mitogen-activated protein kinase (MAPK) pathway leading to a decreased production of NO, iNOS, COX-2 and NF-${\kappa}B$. The results implied the role of RG as an inflammation regulator and its possible application for curing inflammatory diseases.