• 셀메드
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• 제6권4호
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• pp.23.1-23.6
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• 2016

With the rapid developments in nanotechnology, an increasing number of nanomaterials have been applied in various aspects of our lives. Recently, pharmaceutical nanotechnology with numerous advantages has growingly attracted the attention of many researchers. Zinc oxide nanoparticles (ZnO-NPs) are nanomaterials that are widely used in many fields including diagnostics, therapeutics, drug-delivery systems, electronics, cosmetics, sunscreens, coatings, ceramic products, paints, and food additives, due to their magnetic, catalytic, semiconducting, anti-cancer, anti-bacterial, anti-inflammatory, ultraviolet-protective, and binding properties. The present review focused on the recent research works concerning role of ZnO-NP on inflammation. Several studies have reported that ZnO-NP induces inflammatory reaction through the generation of reactive oxygen species by oxidative stress and production of inflammatory cytokines by activation of nuclear factor-${\kappa}B$ ($NF-{\kappa}B$). Meanwhile, other researchers reported that ZnO-NP exhibits an anti-inflammatory effect by inhibiting the up-regulation of inflammatory cytokines and the activation of $NF-{\kappa}B$, caspase-1, $I{\kappa}B$ $kinase{\beta}$, receptor interacting protein2, and extracellular signal-regulated kinase. Previous studies reported that size and shape of nanoparticles, surfactants used for nanoparticles protection, medium, and experimental conditions can also affect cellular signal pathway. This review indicated that the anti-inflammatory effectiveness of ZnO-NP was determined by the nanoparticle size as well as various experimental conditions. Therefore, the author suggests that pharmaceutical therapy with the ZnO-NP is one of the possible strategies to overcome the inflammatory reactions. However, further studies should be performed to maximize the anti-inflammatory effect of ZnO-NP to apply as a potential agent in biomedical applications.

• Journal of Microbiology and Biotechnology
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• 제28권10호
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• pp.1635-1644
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• 2018

Asterias amurensis (starfish) is a marine organism that is harmful to the fishing industry, but is also a potential source of functional materials. The present study was conducted to analyze the profiles of fatty acids extracted from A. amurensis tissues and their anti-inflammatory effects on RAW264.7 macrophage cells. In different tissues, the component ratios of saturated fatty acids, monounsaturated fatty acids, and polyunsaturated fatty acids differed; particularly, polyunsaturated fatty acids such as dihomo-gamma-linolenic acid (20:3n-6) and eicosapentaenoic acid (20:5n-3) were considerably different. In lipopolysaccharide-stimulated RAW264.7 cells, fatty acids from A. amurensis skin, gonads, and digestive glands exhibited anti-inflammatory activities by reducing nitric oxide production and inducing nitric oxide synthase gene expression. Asterias amurensis fatty acids effectively suppressed the expression of inflammatory cytokines such as tumor necrosis $factor-{\alpha}$, interleukin-$1{\beta}$, and interleukin-6 in lipopolysaccharide-stimulated cells. Cyclooxygenase-2 and prostaglandin $E_2$, which are critical inflammation biomarkers, were also significantly suppressed. Furthermore, A. amurensis fatty acids reduced the phosphorylation of nuclear $factor-{\kappa}B$ p-65, p38, extracellular signal-related kinase 1/2, and c-Jun N-terminal kinase, indicating that these fatty acids ameliorated inflammation through the nuclear $factor-{\kappa}B$ and mitogen-activated protein kinase pathways. These results provide insight into the anti-inflammatory mechanism of A. amurensis fatty acids on immune cells and suggest that the species is a potential source of anti-inflammatory molecules.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2018년도 춘계학술발표회
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• pp.91-91
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• 2018

Poncirus Fructus (PF) is obtained by drying the trifoliate orange fruit belonging to the Rutaceae family. In our country of medicine, PF has been used as a treatment of indigestion, allergy and inflammation. But Mechanism and medical data for PF is insignificant. Recently, the effect of the study PF of biological activity was reported, such as anti- thrombosis, anti-bacteria, anti-virus, anti- allergic. We investigated that the effect of PF on anti-inflammatory in murine macrophage-like cell line Raw264.7 cells. Our results show that the expression level of Nitric Oxide (NO) and Matrix-metallopeptidase-9 (MMP-9) significantly decreased. Moreover, to determine the expression level of pro-inflammatory cytokines such as Tumor Necrosis Factor ($TNF-{\alpha}$) and Interleukin-6 (IL-6) and the phosphorylation pattern of signaling molecules of mitogen-activated protein kinase (MAPK) family, we performed ELISA and westren blot in Raw264.7 cells. In addition, nuclear factor-kappa B ($NF-{\kappa}B$) pathway was confirmed. PF extract inhibited the production of $TNF-{\alpha}$ and IL-6. The extract suppressed the phosphorylation of ERK1/2, JNK, and p38 MAPK, and the nuclear translocation of $NF-{\kappa}B$ p65 in activated cells. Our results suggest that PF can be used as a potential therapeutic agent or functional food to relieve inflammation.

• 대한한방내과학회지
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• 제30권1호
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• pp.36-50
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• 2009

Objectives : This study was aimed to verify the cytoprotective function, antioxidative effect and inflammation genes inhibitory effects of Lycium chinense Milie. Therefore the generation of superoxide anion radical ( $O_2\;^-$), peroxynitrite ($ONOO^-$), nitric oxide (NO) and prostaglandin $E_2$ $(PGE_2)$ was investigated in the renal epithelial cells of mouse. Effects of Lycium chinense Milie on the expression of inflammation-related proteins, $IKK-{\alpha}$. $p-IKK-\alpha\beta$, $p-I{\kappa}B-\alpha$, $NF-{\kappa}B$ (p50, p65), COX-2 and iNOS, were examined by western blotting. Methods : For this study, the fluorescent probes were used, namely dihydrorhodamine 123 (DHR 123), 4.5-diaminofluorescein (DAF-2) and 2',7'-dichlorodihydrofluorescein diacetate (DCFDA). Western blotting was performed using anti-$IKK-\alpha$, anti-phospho $IKK-\alpha\beta$, anti-phospho $I{\kappa}B-\alpha$, anti-$NF-{\kappa}B$ (p50, p65), anti-COX-2 and anti-iNOS, respectively. Results : Lyciutn chinense Milie reduced $H_{2}O_{2}$-induced cell death dose-dependently. It inhibited the generation of $O_2\;^-$, $ONOO^-$, NO and $PGE_2$ in the $H_{2}O_{2}$-treated renal epithelial cells of mouse in vitro. Lycium chinense Milie inhibited the expression of $IKK-\alpha$, $p-IKK-\alpha\beta,\;p-I{\kappa}B-\alpha$, COX-2 and iNOS genes by means of decreasing activation of $NF-{\kappa}B$. Conclusions : According to above results. Lycium chinense Milie recommended to be applied in treatment for the inflammatory process and inflammation-related diseases.

• 대한한의학회지
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• 제39권4호
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• pp.40-50
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• 2018

Objectives: The aim of this study is to investigate anti-inflammatory effects of Kyungheechunggan-tang (KHCGT) on LPS- induced RAW 264.7 cells and LX-2 cells and anti-fibrotic effects of KHCGT on LX-2 cells. Materials and Methods: Three types of KHCGTs (KHCGT-A, -B, and -C) by narrowing down the number of constituent herbs from 9 (KHCGT-A) to 5 (KHCGT-B) and to 3 (KHCGT-C) were developed. To understand pharmacological effects of KHCGT, three types of KHCGTs were treated on RAW 264.7 cells and LX-2 cells. Anti-inflammatory activities of KHCGT were evaluated by ELISA assay for pro-inflammatory cytokines, IL-6, $TNF-{\alpha}$ and IL-10, in LPS-stimulated RAW 264.7 cells and for IL-6 production in LPS-induced LX-2 cells. In addition, anti-fibrotic effects of KHCGT were determined by quantitative real-time PCR assay for fibrosis-related genes, ${\alpha}-SMA$, collagen1A1, TIMP1, MMP-2, in LX-2 cells. Results: KHCGT-A and KHCGT-C showed inhibitory effects on secretion of IL-6 in LPS-stimulated RAW 264.7 cells and LX-2 cells. KHCGT-B and KHCGT-C exhibited inhibitory effects on the expression of pro-inflammatory cytokines such as IL-6, $TNF-{\alpha}$, and IL-10 in LPS-stimulated RAW 264.7 cells. The mRNA expression levels of collagen1A1 and MMP-2 were significantly reduced by KHCGT-C whereas TIMP-1 was suppressed by KHCGT-A and KHCGT-B in LX-2 cells. Among three different formulas, KHCGT-C demonstrated the most remarkable effects on inflammation and fibrosis. Conclusions: In this study, KHCGT showed both anti-inflammatory and anti-fibrotic effects which make it to be a prospective agent for chronic liver diseases with inflammation and fibrosis.

• Journal of Ginseng Research
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• 제46권5호
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• pp.675-682
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• 2022

Background: Korean Red Ginseng (KRG) was reported to play an anti-inflammatory role, however, previous studies largely focused on the effects of KRG on priming step, the inflammation-preparing step, and the anti-inflammatory effect of KRG on triggering, the inflammation-activating step has been poorly understood. This study demonstrated anti-inflammatory role of KRG in caspase-11 non-canonical inflammasome activation in macrophages during triggering of inflammatory responses. Methods: Caspase-11 non-canonical inflammasome-activated J774A.1 macrophages were established by priming with Pam3CSK4 and triggering with lipopolysaccharide (LPS). Cell viability and pyroptosis were examined by MTT and lactate dehydrogenase (LDH) assays. Nitric oxide (NO)-inhibitory effect of KRG was assessed using a NO production assay. Expression and proteolytic cleavage of proteins were examined by Western blotting analysis. In vivo anti-inflammatory action of KRG was evaluated with the LPS-injected sepsis model in mice. Results: KRG reduced LPS-stimulated NO production in J774A.1 cells and suppressed pyroptosis and IL-1β secretion in caspase-11 non-canonical inflammasome-activated J774A.1 cells. Mechanistic studies demonstrated that KRG suppressed the direct interaction between LPS and caspase-11 and inhibited proteolytic processing of both caspase-11 and gasdermin D in caspase-11 non-canonical inflammasome-activated J774A.1 cells. Furthermore, KRG significantly ameliorated LPS-mediated lethal septic shock in mice. Conclusion: The results demonstrate a novel mechanism of KRG-mediated anti-inflammatory action that operates through targeting the caspase-11 non-canonical inflammasome at triggering step of macrophage-mediated inflammatory response.

• 동의생리병리학회지
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• 제31권1호
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• pp.75-81
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• 2017

Dangguisoo-san (DGSS), a traditional Korean herbal formula, has been prescribed to patients who suffer from various symptoms related with blood stagnation. Since inflammation can cause blood stagnation, we hypothesized that DGSS suppresses inflammation, relieving the symptoms associated with blood stagnation. In this study, given that DGSS is prepared in a mix of alcohol and water, we prepared the methanol (mDGSS) and water extract (wDGSS) of DGSS and compared their activities in suppressing inflammatory reaction. Western blot analyses show that mDGSS was more effective than wDGSS in activating Nrf2, a key factor that suppresses inflammation. Semi-quantitative RT-PCR shows that mDGSS activating Nrf2 resulted in the induction of Nrf2-dependent genes expression. However, mDGSS was not effective in suppressing the nuclear translocation of $NF-{\kappa}B$, a key factor that promotes inflammation, and the expression of $NF-{\kappa}B$-dependent genes such as TNF-a and IL-1b. When comparing with wDGSS, mDGSS was less effective in suppressing luciferase activity driven by $NF-{\kappa}B$. Therefore, our results show that mDGSS has the anti-inflammatory function by mainly activating Nrf2, while wDGSS does by both activating Nrf2 and suppressing $NF-{\kappa}B$. Our results suggest that preparing DGSS in a mix of water and methanol is a better way to achieve a strong anti-inflammatory efficacy of DGSS.

• 한국응용과학기술학회지
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• 제40권2호
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• pp.244-257
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• 2023

본 연구는 고지방식이를 섭취한 난소절제 쥐의 지방조직에서 제니스테인에 의한 지방조직감소와 항염증에 대한 운동의 영향을 조사하였다. 고지방식이를 섭취한 쥐(C)에 비해 제니스테인 단독처리(G)와 운동 단독처리(Ex)는 지방조직무게, 지방세포 크기 및 혈청 속 포도당과 유리 지방산 수치를 감소시켰으며, 이러한 현상은 제니스테인과 운동을 동시처리(G/Ex) 하였을 경우 더 효과적으로 감소하였다. 지방조직에서 C에 비해 G와 Ex의 지방생성 유전자와 염증성 사이토카인 유전자의 발현은 모두 감소하였고, 특히 이러한 유전자의 감소 현상은 G와 Ex 각각 보다 G/Ex에서 더욱 효과적이었다. 따라서 본 연구는 고지방식이를 섭취한 난소절제 쥐에서 제니스테인과 운동의 동시처리는 제니스테인 단독처리에 비해 더 효과적으로 비만과 지방조직 염증을 개선하였으며 이것은 지방생성 유전자를 긍정적으로 조절한 결과임을 밝혔다. 본 연구는 제니스테인의 항비만과 지방조직 항염증에 대해 운동이 유익한 영향을 미친다는 것을 제안한다.

• IMMUNE NETWORK
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• 제9권1호
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• pp.12-19
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• 2009

Heme oxygenase (HO)-1 is an inducible enzyme that catalyzes the first and rate-limiting step in the oxidative degradation of free heme into ferrous iron, carbon monoxide (CO), and biliverdin (BV), the latter being subsequently converted into bilirubin (BR). HO-1, once expressed during inflammation, forms high concentrations of its enzymatic by-products that can influence various biological events, and this expression is proven to be associated with the resolution of inflammation. The degradation of heme by HO-1 itself, the signaling actions of CO, the antioxidant properties of BV/BR, and the sequestration of ferrous iron by ferritin all concertedly contribute to the anti-inflammatory effects of HO-1. This review focuses on the anti-inflammatory mechanisms of HO-1 actions and its roles in inflammatory diseases.

• Preventive Nutrition and Food Science
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• 제16권4호
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• pp.299-306
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• 2011

The present study was designed to evaluate the inhibitory effects of fermented Liriope platyphylla extract on the production of inflammation-related mediators (NO, ROS, NF-${\kappa}B$, iNOS and COX-2) and pro-inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$, IL-6) in lipopolysaccharide-stimulated RAW 264.7 macrophages. Freeze-dried Liriope platyphylla was fermented by Saccharomyces cerevisiae and extracted with 70% ethanol. In lipopolysaccharide-stimulated macrophage cells, the treatment with fermented Liriope platyphylla extract decreased the generation of intracellular reactive oxygen species dose-dependently and increased antioxidant enzyme activities, including superoxide dismutase, catalase and glutathione peroxidase. Fermented Liriope platyphylla extract also inhibited NO production in lipopolysaccharide-stimulated RAW 264.7 cell. The expressions of NF-${\kappa}B$, iNOS, COX-2 and pro-inflammatory cytokines were inhibited by the treatment with fermented Liriope platyphylla extract. Thus, this study shows the fermented Liriope platyphylla extract could be effective at inhibiting the inflammation process.