• Title/Summary/Keyword: Nuclear factor-kappa

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Anti-inflammatory activity of Ganoderma lucidum by inhibition of NF-κB p65 phosphorylation

  • Kim, Hyung Don;Park, Jeong-Yong;Noh, Hyung-Jun;Lee, Seung Eun;Lee, Jeong Hoon;Seo, Kyung Hye
    • Korean Journal of Agricultural Science
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    • v.46 no.3
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    • pp.653-660
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    • 2019
  • Ganoderma lucidum, an oriental polypore fungus and medicinal mushroom, has a long history of use for promoting health and longevity in Korea, China, and other Asian countries. This study was aimed at determining the anti-inflammatory activity and mechanism of action of Ganoderma lucidum in murine macrophage RAW 264.7 cells. Ganoderma lucidum was extracted with ethanol and freeze-dried. The anti-inflammatory effect (nitrite production) of Ganoderma lucidum extracts was tested using a nitric oxide (NO) colorimetric assay. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was performed to quantify the mRNA expression of cytokines including tumor necrosis factor-${\alpha}$ ($TNF-{\alpha}$), interleukin $(IL)-1{\beta}$, and IL-6. Western blotting was performed to measure the expression levels of inflammation-related proteins, such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor kappa B ($NF-{\kappa}B$) p65, and phosphorylated $NF-{\kappa}B$ p65. The NO colorimetric assay showed that NO production increased with the treatment of lipopolysaccharide in (LPS)-activated RAW 264.7 macrophages and decreased with the cotreatment of Ganoderma lucidum extracts and LPS. Ganoderma lucidum extracts repressed the mRNA expressions of cytokines, which were increased after the LPS treatment. In addition, Ganoderma lucidum extracts inhibited the LPS-induced expression of iNOS and COX-2 and the LPS-induced phosphorylation of $NF-{\kappa}B$ p65. These results suggest that the Ganoderma lucidum extracts exert an anti-inflammatory activity by inhibiting $NF-{\kappa}B$ related proteins and cytokines.

Anti-oxidative and Anti-inflammatory Activities of Decaisnea insignis Ethanol Extract (Decaisnea insignis 에탄올 추출물의 항산화 및 항염증 활성)

  • Jin, Kyong-Suk;Lee, Ji Young;Kwon, Hyun Ju;Kim, Byung Woo
    • Journal of Life Science
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    • v.24 no.9
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    • pp.973-980
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    • 2014
  • This study was conducted to explore new nutraceutical resources from the plant kingdom possessing biological activities. To fulfill this purpose, the anti-oxidative and anti-inflammatory activities of Decaisnea insignis ethanol extract (DIEE) were evaluated. First, DIEE possessed potent scavenging activity against 1,1-diphenyl-2-picryl hydrazyl (DPPH), similar to ascorbic acid used as a positive control. Moreover, DIEE inhibited lipopolysaccharide (LPS)- and hydrogen peroxide ($H_2O_2$)-induced reactive oxygen species (ROS) in RAW 264.7 cells. Furthermore, DIEE induced the expression of an anti-oxidative enzyme, heme oxygenase 1 (HO-1), and its upstream transcription factor, nuclear factor-E2-related factor 2 (Nrf2), in a dose-dependent manner. The modulation of the HO-1 and Nrf2 expressions might be regulated by mitogen-activated protein kinases (MAPKs) and their upstream signaling pathways. On the other hand, DIEE suppressed LPS-induced nitric oxide (NO) formation without cytotoxicity. The inhibition of the NO formation was the result of the downregulation of inducible NO synthase (iNOS) by DIEE. The suppression of NO and iNOS by DIEE might be modulated by their upstream transcription factors, nuclear factor ${\kappa}B$ ($NF-{\kappa}B$), and activator protein 1 (AP-1) pathways. Taken together, these results provide important new insights that D. insignis possesses anti-oxidative and anti-inflammatory activities. Therefore, it might be utilized as a promising material in the field of nutraceuticals.

Anti-inflammatory Activities of Ethylacetate Extract of Rehmannia glutinosa in LPS-induced RAW 264.7 Cells

  • Jin, Chang-Hyun;Lee, Young-Man;Kang, Min-Ah;Park, Yong-Dae;Choi, Dae-Seong;Byun, Myung-Woo;Jeong, Il-Yun
    • Food Science and Biotechnology
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    • v.18 no.4
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    • pp.923-927
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    • 2009
  • This study is to investigate the anti-inflammatory effects of the ethylacetate extract of Rehmannia glutinosa (RGEAE). The anti-inflammatory activities using nitric oxide (NO), cytokine, and chemokine production in lipopolysaccharide (LPS)-induced RAW 264.7 cells were checked. Results indicated that RGEAE suppressed the NO, interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) production in a dose-dependent manner. Inhibition of NO formation was due to a decrease in inducible NOS (iNOS) expression. It was also found that the anti-inflammatory activities of RGEAE resulted from its inhibitory role on the nuclear factor $(NF)-{\kappa}B$ activation and reactive oxygen species (ROS) production. Therefore, it is suggested that RGEAE has potential as a therapeutic material to attenuate the inflammatory disease such as rheumatoid arthritis.

Croton hirtus L'Hér Extract Prevents Inflammation in RAW264.7 Macrophages Via Inhibition of NF-κB Signaling Pathway

  • Kim, Min Jeong;Kim, Ju Gyeong;Sydara, Kong Many;Lee, Sang Woo;Jung, Sung Keun
    • Journal of Microbiology and Biotechnology
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    • v.30 no.4
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    • pp.490-496
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    • 2020
  • Consumption of anti-inflammatory nutraceuticals may help treat or prevent inflammation-related illnesses such as diabetes, cardiovascular disease, and cancer. This study evaluated the effect of Croton hirtus L'Hér extract (CHE) on lipopolysaccharide (LPS)-induced nitric oxide (NO) production and nuclear factor kappa-B (NF-κB) signaling cascades. CHE significantly suppressed LPS-induced NO production and inducible nitric oxide synthase (iNOS) expression in RAW264.7 macrophages, although cyclooxygenase (COX)-2 expression was not affected. CHE also suppressed LPS-induced IκB kinase (IKK), IκB, and p65 phosphorylation in RAW264.7 cells. Western blot and immunofluorescence assays of cytosol and nuclear p65 and the catalytic subunit of NF-κB showed that CHE suppressed LPS-induced p65 translocation from the cytosol to the nucleus. CHE also suppressed LPS-induced Interleukin (IL)-6 and tumor necrosis factor (TNF)-α production in RAW264.7 cells. These results suggest that CHE prevents NO-mediated inflammation by suppressing NF-κB and inflammatory cytokines.

Effects of Baicalin on the Proliferation and Activity of Osteoblastic Cells (Baicalin이 조골세포의 생성 및 활성에 미치는 영향)

  • Ko, Seon-Yle
    • Journal of Oral Medicine and Pain
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    • v.33 no.2
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    • pp.105-110
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    • 2008
  • Baicalin is a flavonoid compound isolated from the medicinal plant Scutellaria baicalensis. It is known to affect multiple biological functions, including of antibacterial, anti-viral, anti-inflammatory and analgesic effects. Baicalin can inhibit nuclear factor-kappaB activation. It has been reported that some flavonoids possess the effects of bone metabolism. The present study was undertaken to determine the possible cellular mechanism of action of baicalin in osteoblasts. The effects on the osteoblast were determined by measuring cell proliferation, cell viability, alkaline phosphatase activity, and osteoprotegerin secretion. Baicalin has no effect on the osteoblastic cell proliferation and cell viability. Baicalin treatment showed increase in alkaline phosphatase activity and osteoprotegerin secretion of osteoblasts. Thus, baicalin may be a regulatory protein within the bone.

Ethanol extract of Synurus deltoides (Aiton) Nakai suppresses in vitro LPS-induced cytokine production in RAW 264.7 macrophages and in vivo acute inflammatory symptoms

  • Jiang, Yunyao;Wang, Myeong-Hyeon
    • Nutrition Research and Practice
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    • v.8 no.1
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    • pp.11-19
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    • 2014
  • Synurus deltoides (Aiton) Nakai, belonging to the Compositae family, is an edible plant widely distributed in Northeast Asia. In this study, we examined the mechanisms underlying the immunomodulative effects of the ethanol extract of S. deltoides (SDE). The SDE extract strongly down-regulated the mRNA expression of the inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and tumour necrosis factor (TNF)-${\alpha}$, thereby inhibiting the production of nitric oxide (NO), prostaglandin E2 (PGE2), and TNF-${\alpha}$ in the lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Furthermore, SDE also suppressed the nuclear translocation of the activation protein (AP)-1 and the nuclear factor-${\kappa}B$ (NF-${\kappa}B$), and simultaneously decreased the phosphorylation of extracellular signal-regulated protein kinases (ERK), p38, and Akt. In agreement with the in vitro observations, the orally administered SDE ameliorated the acute inflammatory symptoms in the arachidonic acid-induced ear edema and the EtOH/HCl-induced gastritis in mice. Therefore, S. deltoides have a potential anti-inflammatory capacity in vitro and in vivo, suggesting the potential therapeutic use in the inflammation-associated disorders.

Inhibition of COX-2 gene expression via $NF-{\kappa}B$ pathway by Ichungwhan (이정환의 $NF-{\kappa}B$ 활성화 기전을 통한 COX-2 저해 기전)

  • Son Myung-yong;Jeong Ji-Cheon
    • The Journal of Korean Medicine
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    • v.25 no.3
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    • pp.90-98
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    • 2004
  • Objectives : The present study was undertaken to investigate the molecular mechanisms of Ichungwhan for inhibition of cyclooxygenase-2 (COX-2) gene expression via suppression of NF-κB (nuclear factor κB) using aged rats. NF-κB is the most important modulator of inflammation and NF-κB regulates the gene expression of several pro-inflammatory cytokines, such as COX-2. Methods : In the experiment, we investigated the scavenging property of Ichungwhan on reactive species (RS) including nitrogen-derived species (RNS), measured by DCF-DA (2,7-dichlorodihydrofluorexcein diacetate) / DHR 123 (dihydrorhodamine 123) assay. Protein expression levels of COX-2, NF-κB, p-ERK and p-p38 were assayed by western blot. Results : We showed that Ichungwhan inhibits RS including RNS and inhibits NF-κB activation by blocking the dissociation of inhibitory IκB-β via suppression of IKK pathway. Also, Ichungwhan inhibits COX-2 gene expression. Conclusions : These findings suggest that Ichungwhan modulates COX-2 gene expression via suppression of the NF-κB pathway.

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Inhibitory Effect of Standardized Curcuma xanthorrhiza Supercritical Extract on LPS-Induced Periodontitis in Rats

  • Kook, Kyo Eun;Kim, Changhee;Kang, Wonku;Hwang, Jae-Kwan
    • Journal of Microbiology and Biotechnology
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    • v.28 no.10
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    • pp.1614-1625
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    • 2018
  • Periodontitis, which is a severe inflammatory disease caused by endotoxins secreted from oral pathogens, destructs gingival tissue and alveolar bone. Curcuma xanthorrhiza, commonly called Java turmeric, has been shown to possess anti-bacterial and anti-inflammatory activities. The present study evaluated the inhibitory effect of C. xanthorrhiza supercritical extract (CXS) standardized with xanthorrhizol on lipopolysaccharide (LPS)-induced periodontitis in an animal model. LPS was topically injected into the periodontium of Sprague-Dawley rats to induce periodontitis and CXS (30 and $100mg{\cdot}kg^{-1}{\cdot}day^{-1}$) was orally administered after day 12. Histologically, CXS inhibited the collapse of gingival tissue by preventing cell infiltration. CXS significantly downregulated the expression of matrix metalloproteases (MMPs) and inflammation-related biomarkers, such as nuclear factor-kappa B ($NF-{\kappa}B$) and interleukin-1 beta ($IL-1{\beta}$) in gingival tissue. CXS also improved bone remodeling by downregulating osteoclastic transcription factors, such as nuclear factor of activated T-cells c1 (NFATc1), tartrate-resistant acid phosphatase (TRAP), and cathepsin K. In addition, CXS upregulated osteoblast differentiation-related markers, alkaline phosphate (ALP) and collagen type I alpha (COLA1). Thus, CXS can ameliorate periodontitis by inhibiting inflammation and improving bone remodeling.

Anti-inflammatory Activity of Fucoidan with Blocking NF-κB and STAT1 in Human Keratinocytes Cells

  • Ryu, Min Ju;Chung, Ha Sook
    • Natural Product Sciences
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    • v.21 no.3
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    • pp.205-209
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    • 2015
  • Fucoidan, a sulfated polysaccharide is found in several types of edible brown algae. It has shown numerous biological activities; however, the molecular mechanisms on the activity against atopic dermatitis have not been reported yet. We now examined the effects of fucoidan on chemokine production co-induced by TNF-α/IFN-γ, and the possible mechanisms underlying these biological effects. Our data showed that fucoidan inhibited the TNF-α/IFN-γ-induced production of thymus and activation-regulated chemokine (TARC) and macrophagederived chemokine (MDC) mRNA in human keratinocytes HaCaT cells. Also, fucoidan suppressed phosphorylation of nuclear factor kappa B (NF-κB) and activation of signal transducer and activator of transcription (STAT)1 in a dose-dependent manner. In addition, fucoidan significantly inhibited activation of extracellular-signal-regulated kinases (ERK) phosphorylation. These data indicate that fucoidan shows anti-inflammatory effects by suppressing the expression of TNF-α/IFN-γ-induced chemokines by blocking NF-κB, STAT1, and ERK1/2 activation, suggestive of as used as a therapeutic application in inflammatory skin diseases, such as atopic dermatitis.