• Title/Summary/Keyword: tumor necrosis factor-kappaB

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Inhibitory Effects of Lycopene on the Expression of Pro-inflammatory Genes in Human Vascular Endothelial Cells (혈관내피세포에서 라이코펜이 염증유전자 발현에 미치는 영향)

  • Kim, Tae-Hoon;Bae, Jong-Sup
    • Food Science and Preservation
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    • v.19 no.2
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    • pp.287-293
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    • 2012
  • Lycopene, found in tomatoes and tomato products, has antioxidant, anticancer, and anti-inflammatory effects. High-mobility-group box 1 (HMGB1) mediates the pro-inflammatory responses in several inflammatory diseases. In this study, the potential roles of lycopene in the HMGB1-mediated pro-inflammatory gene expressions in the primary human-umbilical-vein endothelial cells (HUVECs) were investigated. The data showed that HMGB1 upregulated the expressions of monocyte chemotactic protein 1 (MCP-1), interleukin-6 (IL-6), secretory phospholipase A2 (sPLA2)-IIA, and prostaglandin E2 (PGE2). Lycopene pre-incubation for 6 h decreased the HMGB1-mediated induction of MCP-1, IL-6, sPLA2-IIA, and PGE2. Further study revealed that the inhibitory effects of lycopene on the HMGB-1 induced expression of pro-inflammatory genes were mediated by the inhibition of two important inflammatory cytokines: tumor necrosis factor (TNF)-${\alpha}$ and nuclear factor (NF)-${\kappa}B$. These results suggest that HMGB1 upregulated the expression of pro-inflammatory genes and lycopene inhibited HMGB-1-induced pro-inflammatory genes by inhibiting TNF-${\alpha}$ and NF-${\kappa}B$. This finding will serve as an important evidence in the development of a new medicine for the treatment of inflammatory diseases.

Anti-inflammatory Effects of Ponciri Fructus Extracts on Raw 264.7 Cells

  • Lee, Jin Wook;Jung, Hyuk-Sang;Sohn, Youngjoo;Kang, Yoon Joong
    • Proceedings of the Plant Resources Society of Korea Conference
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    • 2018.04a
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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.

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Anti-inflammatory effect of remifentanil in lipopolysaccharide-stimulated amniotic epithelial cells

  • Kim, Cheul-Hong;Jeong, Seong Soon;Park, Soon Ji;Choi, Eun-Ji;Kim, Yeon Ha;Ahn, Ji-Hye
    • Journal of Dental Anesthesia and Pain Medicine
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    • v.19 no.5
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    • pp.253-260
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    • 2019
  • Background: Sometimes general anesthesia is required for dental surgery in pregnant women. Facial bone fractures or neck abscess should be treated immediately. Dental surgery, however, creates a stressful situation that can cause inflammation. Inflammatory responses are a well-known major cause of preterm labor and preterm birth. Here we demonstrate the effects of remifentanil on the factors related to preterm labor and its mechanism of action on amniotic-derived epithelial cells (WISH cells). Methods: WISH cells were exposed to lipopolysaccharide (LPS) for 24 h and co-treated with various concentrations of remifentanil. MTT assays were performed to measure cell viability. To explain the effects of remifentanil on the factors related to inflammation in WISH cells, activation of nuclear factor kappa B ($NF-{\kappa}B$) and p38 and the expression of interleukin $(IL)-1{\beta}$, tumor necrosis factor $(TNF)-{\alpha}$, cyclooxygenase (COX)2, and prostaglandin E $(PGE)_2$ were quantified using western blotting and RT-PCR, respectively. Results: Remifentanil did not affect WISH cell viability. In western blot analysis, co-treatment with remifentanil resulted in decreased phosphorylation of $NF-{\kappa}B$, and expression of COX2 and $PGE_2$ in LPS-induced inflammation, but the results were statistically significant only at low concentrations. Reduction of $IL-1{\beta}$ and $TNF-{\alpha}$ expression was also observed with RT-PCR. Conclusion: Co-treatment with remifentanil does not affect the viability of WISH cells, but reduces the expression of the factors related to inflammation, which can induce uterine contraction and preterm labor. These findings provide evidence that remifentanil may inhibit uterine contraction and preterm labor in clinical settings.

Ethanol extract separated from Sargassum horneri (Turner) abate LPS-induced inflammation in RAW 264.7 macrophages

  • Sanjeewa, K.K. Asanka;Jayawardena, Thilina U.;Kim, Hyun-Soo;Kim, Seo-Young;Ahn, Ginnae;Kim, Hak-Ju;Fu, Xiaoting;Jee, Youngheun;Jeon, You-Jin
    • Fisheries and Aquatic Sciences
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    • v.22 no.2
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    • pp.6.1-6.10
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    • 2019
  • Background: This study is aimed at identifying the anti-inflammatory properties of 70% ethanol extract produced from an edible brown seaweed Sargassum horneri (SJB-SHE) with industrial-scale production by Seojin Biotech Co. Ltd. S. horneri is a rich source of nutrient and abundantly growing along the shores of Jeju, South Korea. Methods: Here, we investigated the effect of SJB-SHE on LPS-activated RAW 264.7 macrophages. The cytotoxicity and NO production of SJB-SHE were evaluated using MTT and Griess assays, respectively. Additionally, protein expression and gene expression levels were quantified using ELISA, Western blots, and RT-qPCR. Results: Our results indicated that pre-treatment of RAW 264.7 macrophages with SJB-SHE significantly inhibited LPS-induced NO and $PGE_2$ production. SJB-SHE downregulated the proteins and genes expression of LPS-induced iNOS and COX2. Additionally, SJB-SHE downregulated LPS-induced production of pro-inflammatory cytokines (tumor necrosis factor-${\alpha}$, interleukin (IL)-6, and IL-$1{\beta}$). Furthermore, SJB-SHE inhibited nuclear factor kappa-B (NF-${\kappa}B$) activation and translocation to the nucleus. SJB-SHE also suppressed the phosphorylation of mitogen-activated protein kinases (ERK1/2 and JNK). Conclusions: Collectively, our results demonstrated that SJB-SHE has a potential anti-inflammatory property to use as a functional food ingredient in the future.

Suppression of Cyclooxygenase-2 Expression in Colonic Epithelial Cells by Ilekudinol B Isolated from Weigela subsessilis

  • Park, Hye-Jung;Choi, Yeon-A;Tae, Jin;Kang, Chon-Sik;Kim, Dae-Ki;Thuong, Phuong Thien;Kim, Young-Ho;Bae, Ki-Hwan;Lee, Young-Mi
    • Natural Product Sciences
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    • v.12 no.1
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    • pp.38-43
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    • 2006
  • Ilekudinol B is one of the flavonoids isolated from Weigela subsessilis (Caprifoliaceae). In the present study, the suppression effect of ilekudinol B on tumor necrosis factor $(TNF)-{\alpha}-induced$ cyclooxygenase-2 (COX-2) expression was investigated in human colon epithelial cell line HT-29. Interleukin-8 (IL-8) production and prostaglandin $E_2\;(PGE_2)$ secretion was measured by enzyme-linked immunosorbent assay (ELISA). COX-2 and nuclear factor $(NF)-{\kappa}B$ expression were determined by Western blot analysis. Ilekudinol B significantly inhibited $TNF-{\alpha}-induced$ secretion of IL-8 and prostaglandin $E_2\;(PGE_2)$ from the human colon epithelial cell line HT-29 in a concentration-dependent manner. In addition, ilekudinol B remarkably diminished $TNF-{\alpha}-induced$ COX-2 expression and $NF-{\kappa}B$ p65 subunit translocation to the nucleus. In conclusion, our results indicate that ilekudinol B may have anti-inflammatory activity on $TNF-{\alpha}-dependent$ colonic inflammation.

Anti-inflammatory Effects of Belamcanda Chinensis Water Extract (사간 물 추출물의 항염증 효과)

  • Park, Sung-Joo;Kim, Soo-Kon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.24 no.3
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    • pp.410-415
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    • 2010
  • The purpose of this study was to investigate the anti-inflammatory effects of aqueous extract from Belamcanda chinensis (BC) on the RAW 264.7 cells. To evaluate the anti-inflammatory effects of BC, we examined the cytokine productions including nitric oxide (NO), interleukin (IL)-1b, IL-6 and tumor necrosis factor-a (TNF-a) in lipopolysaccharide (LPS)-induced RAW 264.7 cells and also inhibitory mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-kB) using Western blot. BC inhibited LPS-induced production of NO, IL-6 and TNF-a but not of IL-1b in RAW 264.7 cells. BC respectively inhibited the activation of MAPKs such as c-Jun NH2-terminal kinase (JNK) and p38 but not of extracelluar signal-regulated kinase (ERK 1/2) and NF-kB in the LPS-stimulated RAW 264.7 cells. Taken together, Our results showed that BC down-regulated LPS-induced NO, IL-6 and TNF-a productions mainly through JNK and p38 MAPK pathway.

Anti-Inflammatory Activity of Ethanol Extract of Sargassum miyabei Yendo via Inhibition of NF-κB and MAPK Activation (NF-κB와 MAPKs 활성 저해를 통한 미야베 모자반(Sargassum miyabei Yendo) 에탄올 추출물의 항염증 활성)

  • Kim, Min-Ji;Bae, Nan-Young;Kim, Koth-Bong-Woo-Ri;Park, Sun-Hee;Jang, Mi-Ran;Im, Moo-Hyeog;Ahn, Dong-Hyun
    • Microbiology and Biotechnology Letters
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    • v.44 no.4
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    • pp.442-451
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    • 2016
  • The aim of this study was to investigate the anti-inflammatory effect of Sargassum miyabei Yendo ethanol extract (SMYEE) using RAW 264.7 cells and croton oil-induced Balb/c mice. SMYEE inhibited the production of pro-inflammatory cytokines [interleukin (IL)-6, tumor necrosis factor $(TNF)-{\alpha}$, and $IL-1{\beta}$] and nitric oxide in lipopolysaccharide (LPS)-induced inflammatory response. In addition, SMYEE suppressed the expression of inducible nitric oxide, cyclooxygenase-2, and nuclear factor-kappa B. Further, SMYEE inhibited the expression of mitogen-activated protein kinases (MAPKs), such as extra cellular signal-regulated kinase 1/2, p38, and c-Jun N-terminal kinase. In ear edema test, edema formation in the SMYEE treatment was lower than that in the positive control and was similar to that in the prednisolone treatment group. Photomicrographs of mice ear tissue showed a reduction in dermal thickness and number of infiltrated mast cells. Therefore, our results indicate that SMYEE exerts an anti-inflammatory effect via inhibition of nuclear factor ${NF}-{\kappa}B$ and MAPK activation and can be used as a natural source of anti-inflammatory compounds.

Effect of saccharin on inflammation in 3T3-L1 adipocytes and the related mechanism

  • Kim, Hye Lin;Ha, Ae Wha;Kim, Woo Kyoung
    • Nutrition Research and Practice
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    • v.14 no.2
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    • pp.109-116
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    • 2020
  • BACKGROUND/OBJECTIVES: Excessive intake of simple sugars induces obesity and increases the risk of inflammation. Thus, interest in alternative sweeteners as a sugar substitute is increasing. The purpose of this study was to determine the effect of saccharin on inflammation in 3T3-L1 adipocytes. MATERIALS/METHODS: 3T3-L1 preadipocytes were differentiated into adipocytes. The adipocytes were treated with saccharin (0, 50, 100, and 200 ㎍/mL) for 24 h. Inflammation was induced by exposure of treated adipocytes to lipopolysaccharide (LPS) for 18 h and cell proliferation was measured. The concentration of nitric oxide (NO) was measured by using Griess reagent. Protein expressions of nuclear factor kappa B (NF-κB) and inhibitor κB (IκB) were determined by western blot analysis. The mRNA expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin 1β (IL-1β), interleukin 6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-α (TNF-α) were determined by real-time PCR. RESULTS: Compared with the control group, the amount of NO and the mRNA expression of iNOS in the LPS-treated group were increased by about 17.6% and 46.9%, respectively, (P < 0.05), and those parameter levels were significantly decreased by saccharin treatment (P < 0.05). Protein expression of NF-κB was decreased and that of IκB was increased by saccharin treatment (P < 0.05). Saccharin decreased the mRNA expression of COX-2 and the inflammation cytokines (IL-1β, IL-6, MCP-1, and TNF-α) (P < 0.05). CONCLUSIONS: The results of this study suggest that saccharin can inhibit LPS-induced inflammatory responses in 3T3-L1 adipocytes via the NF-κB pathway.

Porcine parvovirus nonstructural protein NS1 activates NF-κB and it involves TLR2 signaling pathway

  • Jin, Xiaohui;Yuan, Yixin;Zhang, Chi;Zhou, Yong;Song, Yue;Wei, Zhanyong;Zhang, Gaiping
    • Journal of Veterinary Science
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    • v.21 no.3
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    • pp.50.1-50.16
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    • 2020
  • Background: Porcine parvovirus (PPV) is a single-stranded DNA virus that causes porcine reproductive failure. It is of critical importance to study PPV pathogenesis for the prevention and control of the disease. NS1, a PPV non-structural protein, is participated in viral DNA replication, transcriptional regulation, and cytotoxicity. Our previous research showed that PPV can activate nuclear factor kappa B (NF-κB) signaling pathway and then up-regulate the expression of interleukin (IL)-6. Objectives: Herein, the purpose of this study is to determine whether the non-structural protein NS1 of PPV also has the same function. Methods: Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay, western blot, immunofluorescence assay and small interfering RNA (siRNA) were used. Results: Our findings demonstrated that PPV NS1 protein can up-regulate the expression levels of IL-6 and tumor necrosis factor-alpha in a dose-dependent manner. Moreover, PPV NS1 protein was found to induce the phosphorylation of IκBα, then leading to the phosphorylation and nuclear translocation of NF-κB. In addition, the NS1 protein activated the upstream pathways of NF-κB. Meanwhile, TLR2-siRNA assay showed TLR2 plays an important role in the activation of NF-κB signaling pathway induced by PPV-NS1. Conclusions: These findings indicated that PPV NS1 protein induced the up-regulated of IL-6 expression through activating the TLR2 and NF-κB signaling pathways. In conclusion, these findings provide a new avenue to study the innate immune mechanism of PPV infection.

Anti-inflammatory Effect of Cheukbaekjurpihwan(CBJPH) (측백저피환(側柏樗皮丸)의 항염(抗炎) 및 면역반응(免疫反應)에 대한 실험적(實驗的) 연구(硏究))

  • Jo, Ok-Hyun;Choi, Chang-Min
    • The Journal of Korean Obstetrics and Gynecology
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    • v.21 no.2
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    • pp.152-165
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    • 2008
  • Purpose: It is the purpose of this study to investigate the anti-inflammatory effects and mechanism of cheukbaekjurpihwan(CBJPH) extract on LPS (lipopolysaccharide)-induced inflammatory mediators in murine peritoneal macrophages. Methods: To evaluate anti-inflammatory effects of CBJPH extract, the production of cytokines(TNF-${\alpha}$(tumor necrosis factor-alpha), IL(interleukin)-6, IL-12) and NO(nitric oxide) was measured in vitro and in vivo. And western blot analysis has been done to look into the mechanism. Results: CBJPH extract reduced LPS-induced NO, TNF-${\alpha}$ and IL-6, IL-12 productions in peritoneal macrophages. CBJPH extract inhibited the activation of JNK(c-Jun N-terminal kinase), but didn't inhibit the activation of MAPKs (mitogen-activated protein kinases) such as p38, ERK1/2(extracelluar signal-regulated kinase1/2) and the degradation of $I_{\kappa}B-{\alpha}$(inhibitory kappa B-alpha) in the LPS-stimulated peritoneal macrophages. CBJPH extract suppressed LPS-induced endotoxin shock and the productions of TNF-${\alpha}$, but not of IL-6, after an oral administration of CBJPH extract Conclusion: CBJPH extract suppressed the productions of LPS-induced NO and cytokines by preventing JNK from phosphorylation, which may provide a clinical basis for anti-inflammatory properties of CBJPH.

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