• Title/Summary/Keyword: $\kappa$

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Brazilin Inhibits of TPA-induced MMP-9 Expression Via the Suppression of NF-${\kappa}B$ Activation in MCF-7 Human Breast Carcinoma Cells

  • Kim, Byeong-Soo
    • Journal of Food Hygiene and Safety
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    • v.25 no.3
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    • pp.209-214
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    • 2010
  • Metastasis is the primary cause of from breast cancer mortality. Cell migration and invasion play important roles in neoplastic metastasis. Matrix metalloproteinase-9 (MMP-9), which degrades the extracellular matrix (ECM), plays an important role in cancer cell invasion. NF-${\kappa}B$ is transcription factor important in the regulation of MMP-9, as the promoter of MMP-9 gene contains binding sites for NF-${\kappa}B$. Brazilin, an active component of sappan wood (Caesalpinia sappan), decreases TPA-induced MMP-9 expression and invasion in MCF-7 cells. Also, brazilin suppressed NF-${\kappa}B$ activation in TPA-treated MCF-7 cells. Taken together, we demonstrated that the inhibition of TPA-induced MMP-9 expression and cell invasion by brazilin is mediated by the suppression of the NF-${\kappa}B$ pathway in MCF-7 cells. This result suggest brazilin provide a potential therapeutic app roach for the treatment of breast cancer.

Structure Activity Relationship of Methylchroman-2-carboxylic Acid N-(Disubstituted)phenylamide Derivatives as Potential NF-${\kappa}B$ Inhibitors (메틸크로만-2-카르복실산 N-(이치환)페닐아마이드 유도체의 NF-${\kappa}B$ 저해 구조-활성 상관 관계)

  • Kim, Tae-Jeong;Kwak, Jae-Hwan;Kim, Young-Soo;Jung, Jae-Kyung;Lee, Hee-Soon
    • YAKHAK HOEJI
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    • v.55 no.2
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    • pp.154-159
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    • 2011
  • During the search for a novel compound that can inhibit NF-${\kappa}B$ activation, 6-hydroxy-7-methoxychroman-2-carboxylic acid phenyl amide (KL-1156) was identified as a good inhibitor of NF-${\kappa}B$ activation. In the present study, we describe the synthesis of methylchroman-2-carboxylic acid N-(disubstituted)phenylamide derivatives (1 and 2 serieses). In addition, their inhibitory effects of NF-${\kappa}B$ are compared with activity of KL-1156 and SAR (structure activity relationship) are explored.

Sulforaphane Inhibits Osteoclastogenesis by Inhibiting Nuclear Factor-κB

  • Kim, Soo-Jin;Kang, So-Young;Shin, Hyun-Hee;Choi, Hye-Seon
    • Molecules and Cells
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    • v.20 no.3
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    • pp.364-370
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    • 2005
  • We show that sulforaphane inhibits osteoclastogenesis in the presence of macrophage colony-stimulating factor (M-CSF) and receptor for activation of nuclear factor-${\kappa}B$ ligand (RANKL) in osteoclast (OC) precursors. Sulforaphane, an aliphatic isothiocyanate, is a known cancer chemo-preventative agent with anti-oxidative properties. Nuclear factor-${\kappa}B$ (NF-${\kappa}B$) is a critical transcription factor in RANKL-induced osteoclastogenesis, and electrophoretic mobility shift assays (EMSAs) and assay of NF-${\kappa}B$-mediated secreted alkaline phosphatase (SEAP) revealed that sulforaphane selectively inhibited NF-${\kappa}B$ activation induced by RANKL. Inhibition may involve interaction of sulforaphane with thiol groups, since it was prevented by reducing agents.

Parameter Design for COBF Based on Kappa-factor Channel Model (Kappa-factor 채널모델에 기반을 둔 최적의 코드북 기반 Opportunistic Beamformer 파라미터 디자인)

  • Kang, Ji-Won;Kwon, Dong-Seung;Lee, Chung-Yong;Hwang, Young-Soo
    • Journal of the Institute of Electronics Engineers of Korea TC
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    • v.45 no.12
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    • pp.20-25
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    • 2008
  • Codebook-based opportunistic beamforming (COBF) technique provides a beam selection diversity to the conventional opportunistic beamforming. In this paper, we design the random matrix and codebook for the COBF technique based on a kappa-factor channel model. Applying the proposed design to the COBF, nearly optimal beams are generated. Therefore, the COBF shows an outstanding performance without regard to the channel correlation related to the kappa-factor.

ent-Kaurane Diterpenoids from Croton tonkinensis Inhibit LPS-induced Transcription Factor NF-${\kappa}{B}$ Activation and NO Production

  • Giang, Phan-Minh;Jin, Hui-Zi;Lee, Jung-Joon
    • Proceedings of the PSK Conference
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    • 2003.04a
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    • pp.120.1-120.1
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    • 2003
  • Nuclear factor-${\kappa}{B}$ (NF-${\kappa}{B}$) belongs to a group of homodimers and heterodimers of Rel/NF-${\kappa}{B}$ proteins that bind to DNA target sites, where they directly regulate gene transcription. The activation of NF-${\kappa}{B}$ has been shown to mediate inflammation and suppress apoptosis. Activated NF-${\kappa}{B}$ has been found n various inflammatory diseases such as rheumatoid arthritis, Atherosclerosis, asthma, nflammatory bowel disease, and Helicobacter pylori-associated gastritis and associated with cancer, cachexia, diabetes, euthyroid sick syndrome, and AIDS. (omitted)

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Simple modeling to explore temperatures, heated temperature, and Kappa values of a current sheet observation

  • Lee, Jin-Yi;Raymond, John C.;Reeves, Katharine K.;Shen, Chengcai;Kahler, Stephen;Moon, Yong-Jae;Kim, Yeon-Han
    • The Bulletin of The Korean Astronomical Society
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    • v.46 no.2
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    • pp.79.2-79.2
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    • 2021
  • We explore the range of possibilities of temperatures, heated temperature, and Kappa values of a current sheet observation on 2017 September 10. First, we construct a grid model with rapid heating (Theat) and various Kappa (κ) values. We assume a simple density model and use adiabatic cooling to set the temperature during expansion. Next, we calculate the ion fractions using a time-dependent ionization model with adiabatic cooling and various Kappa values. The calculated ion fractions are used to simulate the DNs of the Atmospheric Imaging Assembly on board the Solar Dynamic Observatory. Then, we explore the possible range of the temperatures and Kappa values, comparing the simulated images with the observations. Finally, we discuss the range of the heated temperature and Kappa values and whether the result of this study suggests continuous heating of the current sheet plasma during the expansion.

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Anti-inflammation effect of rebaudioside A by inhibition of the MAPK and NF-κB signal pathway in RAW264.7 macrophage (RAW264.7 대식세포에서 MAPK 및 NF-κB 신호전달 억제를 통한 rebaudioside A의 항염 효과)

  • Choi, Da Hee;Cho, Uk Min;Hwang, Hyung Seo
    • Journal of Applied Biological Chemistry
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    • v.61 no.2
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    • pp.205-211
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    • 2018
  • Rebaudioside A is a natural sweetener isolated from Stevia rebaudiana Bertoni, one of the glycosides based on steviol. Recent studies have shown that rebaudioside A inhibits the inflammatory response by inhibiting cytokines secretion such as interleukin-$1{\alpha}/1{\beta}$ in activated RAW264.7 mouse macrophage cells by LPS. However, the inhibitory mechanism of inflammation by rebaudioside A in the presence of LPS has not been fully elucidated. Therefore, in this study, we tried to investigate the anti-inflammatory activity of rebaudioside A at the protein level when RAW264.7 cells were stimulated by LPS. The inducible nitric oxide synthase protein expression level was reduced in the group treated with $250{\mu}M$ rebaudioside A compared to the LPS-treated group. In addition, the mRNA expression level of $NF-{\kappa}B$, which is a representative nuclear transcription factor by inflammatory signal, was also decreased as compared with that of LPS-treated group. In addition, $NF-{\kappa}B$ and inhibitor-${\kappa}B$ ($I-{\kappa}B$) complexes that are known to be dissociated by $I-{\kappa}B$ phosphorylation and ubiquitination were less phosphorylated than LPS treated group in the presence rebaudioside A. Finally, we could find that rebaudioside A was involved in the $NF-{\kappa}B$ pathway through reducing extracellular signal-regulated kinase1/2 phosphorylation in a concentration-dependent manner. These results suggest that rebaudioside A might suppress inflammatory reaction through MAPK and $NF-{\kappa}B$ regulation in LPS-stimulated RAW264.7.

Antiinflammatory Effect of Lactic Acid Bacteria: Inhibition of Cyclooxygenase-2 by Suppressing Nuclear Factor-${\kappa}B$ in Raw264.7 Macrophage Cells

  • Lee, Jeong-Min;Hwang, Kwon-Tack;Jun, Woo-Jin;Park, Chang-Soo;Lee, Myung-Yul
    • Journal of Microbiology and Biotechnology
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    • v.18 no.10
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    • pp.1683-1688
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    • 2008
  • Lactobacillus casei 3260 (L. casei 3260) was evaluated in relation to the inflammatory response mediated by lipopolysaccharide (LPS)-induced nuclear factor-${\kappa}B$ (NF-${\kappa}B$) and cyclooxygenase-2 (COX-2) expression in Raw264.7 macrophage cells. The treatment of Raw264.7 cells with L. casei 3260 significantly inhibited the secretion of tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and prostaglandins $E_{2}\;(PGE_{2})$, followed by suppression of COX-2. To clarify the molecular mechanism, the inhibitory effect of L. casei 3260 on the NF-${\kappa}B$ signaling pathway was examined based on the luciferase reporter activity. Although the treatment of Raw264.7 cells with L. casei 3260 did not affect the transcriptional activity of NF-${\kappa}B$, it did inhibit NF-${\kappa}B$ activation, as determined by the cytosolic p65 release and degradation of I-${\kappa}B{\alpha}$. Therefore, these findings suggest that the suppression of COX-2 through inhibiting the NF-${\kappa}B$ activation by LPS may be associated with the antiinflammatory effects of L. casei 3260 on Raw264.7 cells.

Anti-inflammatory Effects of Flavokavain C from Kava (Piper methysticum) Root in the LPS-induced Macrophages (LPS로 유도된 대식세포에서 카바뿌리로부터 분리한 Flavokavain C의 항염증 효과)

  • Park, Chung;Han, Jong-Min
    • Journal of the Society of Cosmetic Scientists of Korea
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    • v.42 no.4
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    • pp.311-320
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    • 2016
  • Kava (Piper methysticum, P. methysticum) is used as traditional herbal medicine for urogenital diseases, rheumatisms, gastrointestinal problems, respiratory irritations, and pulmonary pains. We identified a flavokavain C (FKC) from P. methysticum, which showed anti-inflammatory activity on nuclear factor ${\kappa}B$ (NF-${\kappa}B$)-dependent nitric oxide (NO) production and expression of inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-induced RAW264.7 macrophages. FKC inhibited accumulation of reactive oxygen species (ROS), such as hydrogen peroxide, and was able to dose-dependently reduce the LPS-induced NO production and the expression of various inflammation-associated genes (iNOS, IL-$1{\beta}$, IL-6) through inhibition of NF-${\kappa}B$ and MAPKs (ERK and JNK). In conclusion, these results indicate that FKC may have the potential to prevent inflammation process including NF-${\kappa}B$ and MAPKs pathways, and it could be applicable to functional cosmetics for anti-inflammation and antioxidant properties.

Salicylate Regulates Cyclooxygenase-2 Expression through ERK and Subsequent $NF-_kB$ Activation in Osteoblasts

  • Chae, Han-Jung;Lee, Jun-Ki;Byun, Joung-Ouk;Chae, Soo-Wan;Kim, Hyung-Ryong
    • The Korean Journal of Physiology and Pharmacology
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    • v.7 no.4
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    • pp.239-246
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    • 2003
  • The expression of cyclooxygenase-2 (COX-2) is a characteristic response to inflammation and can be inhibited with sodium salicylate. $TNF-{\alpha}$ plus $IFN-{\gamma}$ can induce extracellular signal-regulated kinase (ERK), IKK, $I{\kappa}B$ degradation and NF-${\kappa}B$ activation. The inhibition of the ERK pathway with selective inhibitor, PD098059, blocked cytokine-induced COX-2 expression and $PGE_2$ release. Salicylate treatment inhibited COX-2 expression induced by $TNF-{\alpha}$/$IFN-{\gamma}$ and regulated the activation of ERK, IKK and $I{\kappa}B$ degradation and subsequent NF-${\kappa}B$ activation in MC3T3E1 osteoblasts. Furthermore, antioxidants such as catalase, N-acetyl-cysteine or reduced glutathione attenuated COX-2 expression in combined cytokines-treated cells, and also inhibited the activation of ERK, IKK and NF-${\kappa}B$ in MC3T3E1 osteoblasts. In addition, $TNF-{\alpha}$/$IFN-{\gamma}$ stimulated ROS release in the osteoblasts. However, salicylate had no obvious effect on ROS release in DCFDA assay. The results showed that salicylate inhibited the activation of ERK and IKK, $I{\kappa}B$ degradation and NF-${\kappa}B$ activation independent of ROS release and suggested that salicylate exerts its anti-inflammatory action in part through inhibition of ERK, IKK, $I{\kappa}B$, $NF-{\kappa}B$ and resultant COX-2 expression pathway.