• 대한본초학회지
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• 제26권4호
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• pp.31-37
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• 2011

Objectives : Chrysanthemum boreale flower is widely distributed in Korea, Japan, China, and Eastern countries. C. boreale flower is also one of the herbs used for the treatment of various inflammatory disease in Korean Medicine. So, this research was designed to study anti-inflammatory effect of C. boreale flower and its mechanism. Methods : We investigated nitro oxide (NO) and prostaglandin $E_2$ ($PGE_2$) production by ELISA. And expressions of inducible nitric oxide synthase (iNOS), Cyclooxygenase-2 (COX-2) and nuclear factor-${\kappa}B$ P50/65 (NF-${\kappa}B$ P50, NF-${\kappa}B$ P65) were measured in RAW 264.7 murine macrophage cells induced by LPS. Results : MeOH ex., EtOAc fr., $CHCl_3$ fr. and Water fr. of C. boreale flower showed anti-inflammatory effect through inhibition of NO and PGE expression respectively. Among them, EtOAc fr. and $CHCl_3$ fr. inhibited production of NO and $PGE_2$ through inhibition of iNOS and COX-2 expression. And MeOH ex., EtOAc fr. and $CHCl_3$ fr. inhibited translocation of NF-${\kappa}B$ P65, NF-${\kappa}B$ P50 by inhibiting phosphrylation of $I{\kappa}B$. Conclusions : MeOH ex. EtOAc fr, $CHCl_3$ fr., and Water fr. of the C. boreale flower have anti-inflammatory activity.

• Toxicological Research
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• 제24권1호
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• pp.17-22
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• 2008

Sopungsan (SS) is a traditional Korean decoction used for the treatment of dermatitis. The aim of this study is to confirm whether or not SS has a preventive effect on the development of atopic dermatitis in dinitrochlorobenzene-applied Nc/Nga mice. SS was administered orally to Nc/Nga mice, which led to the remarkable suppression of the development of dermatitis, as determined by a histological examination and the serum IgE levels. Moreover, SS inhibited the production of thymus- and activation-regulated chemokine (TARC) and its mRNA expression in a keratinocyte cell line, HaCaT, which had been stimulated with tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interferon-${\gamma}$ (IFN-${\gamma}$). Activation of the nuclear factor-${\kappa}B$ (NF-${\kappa}B$) or activator protein-1 (AP-1) is one of key steps in the signaling pathways mediating induction of TARC. In this study, SS selectively suppressed NF-${\kappa}B$ activation which may be essential for TARC expression in $TNF-{\alpha}/IFN-{\gamma}$ treated keratinocytes. The inhibitory effect of SS on NF-${\kappa}B$ activation and TARC production might be associated with the anti-dermatitic effects of SS.

• Natural Product Sciences
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• 제14권3호
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• pp.206-213
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• 2008

This study was designed to investigate the anti-inflammatory effects of mangiferin isolated from the rhizome of Anemarrhena asphodeloides, a natural polyphenol, on lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. Mangiferin dose-dependently inhibited LPS-induced nitric oxide (NO) and prostaglandin $E_2\;(PGE_2)$ productions in RAW 264.7 macrophages and peritoneal macrophages isolated from C57BL/6 mice. Consistent with these data, mangiferin suppressed the LPS-induced expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein and mRNA levels in a concentration-dependent manner, as determined by Western blotting and RT-PCR, respectively. In addition, the release of tumor necrosis $factor-{\alpha}$($TNF-{\alpha}$) and interleukin-6 (IL-6), and the mRNA expression levels of these cytokines were reduced by mangiferin in a dose-dependent manner. Moreover, mangiferin effectively inhibited the transcriptional activation of nuclear factor-kappa B $(NF-{\kappa}B)$. These results suggest that the anti-inflammatory properties of mangiferin are caused by iNOS, COX-2, $TNF-{\alpha}$, and IL-6 down-regulation due to $(NF-{\kappa}B)$ inhibition in RAW 264.7 macrophages.

• 동의생리병리학회지
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• 제21권2호
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• pp.498-503
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• 2007

Inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 are important inflammatory mediators that have been implicated in pathogenesis of inflammation and certain types of human cancers. The present study was designed in order to determine whether Wild ginseng (Panax ginseng C. A. Mayer) could modulate $I{\kappa}B$-kinase (IKK), iNOS and COX-2 gene expression and its immune responses in RAW 264.7 macrophages stimulated with lipopolysaccharide (LPS, 1 ${\mu}/m{\ell}$). Wild ginseng extract dose-dependantly (*0.5 - 2 ${\mu}/m{\ell}$) decreased the LPS-induced IKK, iNOS and COX-2 mRNA expression and its immune responses. Moreover, it inhibited unclear factor (NF)-${\kappa}B$ immune response by LPS. These data be likely to indicate that Wild ginseng may acts as inflammatory regulator and may be possible to develope a useful agent for inflammatory diseases.

• 한방비만학회지
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• 제16권2호
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• pp.79-84
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• 2016

Objectives: The purpose of this study was to observe the effects of Citri Reticulatae Viride Pericarpium (CP) on 4-Hydroxynonenal (4-HNE)-induced inflammation in PC12 cells. Methods: 4-HNE was treated in PC12 cell to cause inflammatory response, and then treated with CP water extract at 25, 50, and $100{\mu}g/ml$. The phosphorylation of Jun N-terminal kinase (JNK) and the expression of $NF-{\kappa}B$ in PC12 cells were determined by Western blot, respectively. Results: The phosphorylation of JNK was significantly decreased in 4-HNE-stimulated PC12 cell by the treatment of CP extract at $25{\mu}g/ml$. The 4-HNE-induced expression of nuclear factor kappa-light-chain-enhancer of activated B cells ($NF-{\kappa}B$) p65 in nuclear of the cells was significantly decreased in PC12 cell by treatment with CP extract at 25, 50, and $100{\mu}g/ml$. Conclusions: These results suggest that CP water extract has an anti-inflammatory activity through suppressing the JNK and $NF-{\kappa}B$ activation.

• 한국자원식물학회지
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• 제27권3호
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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.

• 한국식품과학회지
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• 제44권6호
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• pp.759-762
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• 2012

이번 실험을 통하여 PEIC가 OVA에 의해 유도된 NF-${\kappa}B$ 활성과 iNOS, COX-2 발현에 어떠한 영향을 미치는지 알아 보았다. PEIC는 OVA에 의해 유도된 NF-${\kappa}B$ 활성을 억제시켰다. 또한 PEIC는 OVA에 의해 유도된 iNOS의 발현도 억제시켰다. 하지만 PEIC는 OVA에 의해 유도된 COX-2 발현은 억제시키지 못하였다. 이러한 결과는 iNOS와 COX-2가 서로 다른 메커니즘에 의해 조절된다는 것을 암시한다. 또한 PEIC는 알러지와 같은 만성적인 질병들을 조절할 수 있는 치료제 개발 및 백신 제조에 중요한 역할을 할 것으로 기대한다.

• Parasites, Hosts and Diseases
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• 제49권3호
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• pp.291-294
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• 2011

Trichomonas vaginalis is a flagellated lumen-dwelling extracellular protozoan parasite that causes human trichomoniasis via sexual intercourse. Human neutrophils play a crucial role in acute tissue inflammatory responses in T. vaginalis infection. In this study, we investigated the signaling mechanism of neutrophil responses when stimulated with T. vaginalis-derived secretory products (TvSP), which were collected from $1{\times}10^7$ live trichomonads. Incubation of human neutrophils isolated from peripheral blood with TvSP induced up-regulation of IL-8 protein secretion. In addition, stimulation with TvSP induced phosphorylation of NF-${\kappa}B$ and CREB in neutrophils. Moreover, TvSP-induced IL-8 production was also significantly inhibited by pretreatment of neutrophils with $i{\kappa}B$ inhibitor or CREB inhibitor. These results suggest that transcription factors NF-${\kappa}B$ and CREB are involved in IL-8 production in human neutrophils induced by stimulation with T. vaginalis infection.

• 대한한방부인과학회지
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• 제30권2호
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• pp.1-15
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• 2017

Objectives: The object of this study was to identify the anti-inflammatory effects of Patrinia scabiosaefolia aqueous extract (PSE). Methods: RAW 264.7 cells were pre-treated with PSE and then incubated with or without lipopolysaccharide (LPS). Cell viability, production of nitric oxide (NO), secretion of pro-inflammatory cytokine, activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-${\kappa}B$) were measured. In addition, we observed mice survival rate after LPS and their cytokine levels of serum. We also observed inflammatory and hemorrhagic change on the histological sections of the liver. Results: PSE inhibited LPS-induced NO production, interleukin (IL)-6 secretion, c-Jun NH2-terminal kinase (JNK) and NF-${\kappa}B$ activation. In addition, PSE reduced the death rate of LPS-induced mice and IL-6 production on the serum of mice. PSE inhibited inflammation and hemorrhage on liver tissue as well. Conclusions: The results suggest that PSE have anti-inflammatory effects by inhibited NF-${\kappa}B$ and JNK activation, IL-6 secretion, and NO production. So PSE may be effective treatment for the inflammatory disease.

• Molecules and Cells
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• 제41권12호
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• pp.1008-1015
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• 2018

$I{\kappa}B$, a cytoplasmic inhibitor of nuclear factor-${\kappa}B$ ($NF-{\kappa}B$), is reportedly degraded via the proteasome. However, we recently found that long-term incubation with proteasome inhibitors (PIs) such as PS-341 or MG132 induces $I{\kappa}B{\alpha}$ degradation via an alternative pathway, lysosome, which results in $NF-{\kappa}B$ activation and confers resistance to PI-induced lung cancer cell death. To enhance the anti-cancer efficacy of PIs, elucidation of the regulatory mechanism of PI-induced $I{\kappa}B{\alpha}$ degradation is necessary. Here, we demonstrated that PI up-regulates nuclear factor (erythroid-derived 2)-like 2 (Nrf2) via both de novo protein synthesis and Kelch-like ECH-associated protein 1 (KEAP1) degradation, which is responsible for $I{\kappa}B{\alpha}$ degradation via macroautophagy activation. PIs increased the protein level of light chain 3B (LC3B, macroautophagy marker), but not lysosome-associated membrane protein 2a (Lamp2a, the receptor for chaperone-mediated autophagy) in NCI-H157 and A549 lung cancer cells. Pretreatment with macroautophagy inhibitor or knock-down of LC3B blocked PI-induced $I{\kappa}B{\alpha}$ degradation. PIs up-regulated Nrf2 by increasing its transcription and mediating degradation of KEAP1 (cytoplasmic inhibitor of Nrf2). Overexpression of dominant-negative Nrf2, which lacks an N-terminal transactivating domain, or knock-down of Nrf2 suppressed PI-induced LC3B protein expression and subsequent $I{\kappa}B{\alpha}$ degradation. Thus, blocking of the Nrf2 pathway enhanced PI-induced cell death. These findings suggest that Nrf2-driven induction of LC3B plays an essential role in PI-induced activation of the $I{\kappa}B$/$NF-{\kappa}B$ pathway, which attenuates the anti-tumor efficacy of PIs.