• Herbal Formula Science
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• v.18 no.1
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• pp.105-120
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• 2010

Paeonia Suffruticosa and Prunus Persica have been used as oriental medicine for removal of fever, alleviation of pain, an anti-phlogistic effect and removal of extravasated blood. However, it has been never shown the effects of these herbal medicines on anti-inflammatory processes. This experiment was performed to show how these herbs could act as anti-inflammatory medicines at cellular level. Anti-inflammation effects of water extracts from Paeonia Suffruticosa and Prunus Persica as well as their mixture have been investigated, and the results were follows; 1) each extract slightly suppressed the expression and production of inflammatory mediators and enzymes such as NO, iNOS, IL-$1{\beta}$, and TNF-$\alpha$ in lipopolysaccharid(LPS)-stimulated RAW264.7 cells and mouse primary peritoneal macrophages in a dose-dependent manner. These suppressive effects, however, were synergistically increased by their mixture. 2) Each extract of Paeonia Suffruticosa and Prunus Persica insignificantly suppressed the activation and activity of NF-${\kappa}B$ in LPS-stimulated RAW264.7 cells, which controls the expression of inflammatory mediators such as NO, iNOS, IL-$1{\beta}$, and TNF-$\alpha$. However, extract mixture of Paeonia Suffruticosa and Prunus Persica suppressed effectively the activation and activity of NF-${\kappa}B$. 3) Each of Paeonia Suffruticosa and Prunus Persica induced translocation of NF-${\kappa}B$ to the nucleus from the cytosol and DNA-binding activity of nuclear NF-${\kappa}B$ in LPS-activated RAW264.7 cells. The extract mixture of Paeonia Suffruticosa and Prunus Persica showed more significant suppression of the NF-${\kappa}B$ translocation and its DNA-binding activity, as compared to those of the each extract. These results suggest that the extract mixture of Paeonia Suffruticosa and Prunus Persica may affect different control mechanisms for NF-${\kappa}B$ activation and the expression and production of NF-${\kappa}B$-dependent inflammatory mediators, indicating that this extract mixture may be useful for treatment of inflammatory diseases.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.20 no.2 s.33
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• pp.89-101
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• 2007

Objectives : This study was carried out to investigate the effects of Jeondo-San(JDS) on anti-Inflammation and anti-Propionibacterium acnes. Methods : The effects of JDS on anti-Inflammation and anti-Propionibacterium acnes were measured by the cytotoxicity of Raw 264.7 cell, the inhibition for NO, $TNF-{\alpha}$, $PGE_2$, iNOS and COX-2, the blocking $NF-{\kappa}B$ into nucleus and the sterilizing power for Propionibacterium acnes. Results : 1. All concentrations of JDS has no cytotoxicity in Raw 264.7 cell. 2. All concentrations of JDS inhibited the production of NO in the Raw 264.7 cell stimulated with LPS. 3. All concentrations of JDS did not significantly inhibit the production of $TNF-{\alpha}$ in the Raw 264.7 cell stimulated with LPS. 4. All concentrations of JDS inhibited the production of $PGE_2$ in the Raw 264.7 cell stimulated with LPS. 5. All concentrations of JDS did not inhibit the expression of COX-2 but concentrations of 50\;{\mu}g/ml$, 100\;{\mu}g/ml$ JDS inhibited iNOS expression in the Raw 264.7 cell stimulated with LPS. 6. Concentrations of 50\;{\mu}g/ml$, 100\;{\mu}g/ml$ JDS has the effect of blocking $NF-{\kappa}B$ into nucleus in LPS-induced macrophage Raw 264.7 cell. 7. All concentrations of IDS did not have the inhibitory effect of Propionibactrium acnes. Conclusions : The present date suggest that JDS has a effect on the stage of inflammation of acne.

• Archives of Pharmacal Research
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• v.25 no.5
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• pp.691-696
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• 2002

Doxorubicin (DOX) is an active and broad spectrum chemotherapeutic agent. Increased inducible nitric oxide synthase (NOS) expression and/or activity have been reported in several human tumors. While the relationship between DOX treatment and the enzymatic activity of endothelial NOS has been well characterized, little is known about the effects of DOX on the expression of iNOS in human cancer cells. In the present study, we characterized the effects of DOX on the nitric oxide (NO) production by colorectal cancer cells, DLD-1. IFN-${\gamma}$/IL-1$\beta$ (CM) increased the production of NO, whereas pretreatment of DOX inhibited the production of NO in response to CM in a dose dependent manner. The increased expressions of iNOS mRNA and protein by CM were completely blocked by DOX without affecting the iNOS mRNA stability. However, DOX activated nuclear factor-kB (NF-kB) in response to CM. Furthermore, the expression of inhibitor kB$\alpha$ was reduced by DOX in a dose dependent manner. Collectively, DOX inhibited the production of NO by DLD-1 cells, which is not linked to well known transcription factor, NF-kB. Therefore, further studies on the possible mechanisms of inhibitory effects of NO production by DOX would be worth pursuing.

• Korean Journal of Food Science and Technology
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• v.51 no.3
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• pp.278-285
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• 2019

Tomato (Lycopersicon esculentum) is widely known for its beneficial effects on human health. To investigate the beneficial effects of polysaccharides from cherry tomato, cherry tomato polysaccharides (CTP) were prepared, the component sugars were analyzed, and the immunomodulatory activities in RAW 264.7 macrophages were assessed. CTP mainly contained arabinose (Ara) and galactose (Gal), suggesting that CTP might be enriched with an arabinogalactan (AG) moiety. The Ara and Gal present in CTP are likely components of AG-II (35.4%), namely $arabino-{\beta}-(3,6)-galactan$. To investigate the immunomodulatory activity of CTP, cytokine levels and iNOS2, COX-2, and $NF-{\kappa}B$ protein levels were analyzed, and $NF-{\kappa}B$ nuclear translocation and phagocytosis were observed by immunofluorescence. CTP significantly increased the levels of $TNF-{\alpha}$, MCP-1, and IL-6. CTP also increased iNOS2 and COX-2 expression as well as $NF-{\kappa}B$ nuclear translocation in RAW 264.7 cells. CTP significantly stimulated phagocytosis activity. These results showed that CTP stimulates macrophage activity, which can boost the innate immune response. CTP with high AG-II content could be used as a prebiotic to strengthen immunity.

• BMB Reports
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• v.48 no.3
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• pp.172-177
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• 2015

Upregulation of pro-inflammatory mediators contributes to ${\beta}$-cell destruction and enhanced infiltration of immune cells into pancreatic islets during development of type 1 diabetes mellitus. In this study, we examined the regulatory effects and the mechanisms of action of celastrol against cytotoxicity and pro-inflammatory immune responses in the RINm5F rat pancreatic ${\beta}$-cell line stimulated with a combination of interleukin-1 beta, tumor necrosis factor-alpha, and interferon-${\gamma}$. Celastrol significantly restored cytokine-induced cell death and significantly inhibited cytokine-induced nitric oxide production. In addition, the protective effect of celastrol was correlated with a reduction in pro-inflammatory mediators, such as inducible nitric oxide synthase, cyclooxygenase-2, and CC chemokine ligand 2. Furthermore, celastrol significantly suppressed cytokine-induced signaling cascades leading to nuclear factor kappa B (NF-${\kappa}B$) activation, including $I{\kappa}B$-kinase (IKK) activation, $I{\kappa}B$ degradation, p65 phosphorylation, and p65 DNA binding activity. These results suggest that celastrol may exert its cytoprotective activity by suppressing cytokine-induced expression of pro-inflammatory mediators by inhibiting activation of NF-${\kappa}B$ in RINm5F cells.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.2
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• pp.194-201
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• 2016

The anti-inflammatory activity of ethanol extract from Chondrus nipponicus Yendo (CNYEE) was investigated by measuring production of a lipopolysaccharide-induced inflammatory response mediator. CNYEE had no cytotoxic effects on proliferation of macrophages compared to the control. CNYEE significantly inhibited (over 50%) NO production at $50{\mu}g/mL$, with inhibitory effects on expression levels of cytokines such as interleukin (IL)-6, tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), and IL-$1{\beta}$. In particular, IL-6 inhibitory activity of CNYEE was higher than 70% at $100{\mu}g/mL$. CNYEE also reduced protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor (NF)-${\kappa}B$ in a dose-dependent manner. CNYEE also significantly reduced phosphorylation of p38, extracellular signal-regulated kinase, and c-Jun N-terminal kinase. Therefore, these results suggest that CNYEE may have anti-inflammatory effects by modulating the NF-${\kappa}B$ and mitogen-activated protein kinases signaling pathways and may be used as an anti-inflammatory therapeutic material.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.4
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• pp.379-389
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• 2018

A nucleobase adenine is a fundamental component of nucleic acids and adenine nucleotides. Various biological roles of adenine have been discovered. It is not produced from degradation of adenine nucleotides in mammals but produced mainly during polyamine synthesis by dividing cells. Anti-inflammatory roles of adenine have been supported in IgE-mediated allergic reactions, immunological functions of lymphocytes and dextran sodium sulfate-induced colitis. However adenine effects on Toll-like receptor 4 (TLR4)-mediated inflammation by lipopolysaccharide (LPS), a cell wall component of Gram negative bacteria, is not examined. Here we investigated anti-inflammatory roles of adenine in LPS-stimulated immune cells, including a macrophage cell line RAW264.7 and bone marrow derived mast cells (BMMCs) and peritoneal cells in mice. In RAW264.7 cells stimulated with LPS, adenine inhibited production of pro-inflammatory cytokines $TNF-{\alpha}$ and IL-6 and inflammatory lipid mediators, prostaglandin $E_2$ and leukotriene $B_4$. Adenine impeded signaling pathways eliciting production of these inflammatory mediators. It suppressed $I{\kappa}B$ phosphorylation, nuclear translocation of nuclear factor ${\kappa}B$ ($NF-{\kappa}B$), phosphorylation of Akt and mitogen activated protein kinases (MAPKs) JNK and ERK. Although adenine raised cellular AMP which could activate AMP-dependent protein kinase (AMPK), the enzyme activity was not enhanced. In BMMCs, adenine inhibited the LPS-induced production of $TNF-{\alpha}$, IL-6 and IL-13 and also hindered phosphorylation of $NF-{\kappa}B$ and Akt. In peritoneal cavity, adenine suppressed the LPS-induced production of $TNF-{\alpha}$ and IL-6 by peritoneal cells in mice. These results show that adenine attenuates the LPS-induced inflammatory reactions.

• Journal of Applied Biological Chemistry
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• v.62 no.1
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• pp.57-66
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• 2019

The ethyl acetate fraction of Bat Faeces (Ye Ming Sha: natural products used in Chinese Medicine) after fermentation (EFBF-AF) showed enhanced anti-oxidative effects in 2,2-diphenyl-1-picrylhydrazyl and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt assays. Fermentation of the Bat Faeces by using the crude enzyme extract from Aspergillus kawachii, significantly increased the anti-inflammatory effects. Fermented Bat Faeces markedly inhibited nitric oxide production, inducible nitric oxide synthase, and cyclooxygenase-2 expression in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. The EFBF-AF reduced the nuclear translocation of nuclear factor kappa B ($NF-{\kappa}B$) via $IKK{\alpha}$ and $I{\kappa}B{\alpha}$ phosphorylation, and decreased the phosphorylated the extracellular signal-regulated kinases (ERK) and p38 expression in LPS-treated RAW 264.7 macrophages. In addition, the EFBF-AF suppressed the expression of pro-inflammatory genes, such as interleukin-$1{\beta}$, interleukin-6, and tumor necrosis $factor-{\alpha}$. These results suggest that fermented Bat Faeces may suppress pro-inflammatory responses in LPS-stimulated RAW 264.7 macrophages cells via ERK, p38 mitogen-activated protein kinase and $NF-{\kappa}B$ signaling pathways.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.1
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• pp.78-82
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• 2013

It has been reported that Scolopendra morsitans L.(SML) has beneficial effects on human health and diverse diseases. The purpose of this study was to investigate the anti-inflammatory effects of ether extract from Scolopendra morsitans L. on lipopolysaccharide(LPS)-induced inflammatory response. Thus, we examined the inhibitory effect of SML ether fraction on LPS-induced increase of inflammatory mediators(NO, iNOS, COX-2, and $I{\kappa}B{\alpha}$) and pro-inflammatory cytokines(TNF-${\alpha}$) in RAW 264.7 cells. In the present study, SML ether extract itself decreased cell viability in a dose dependent manner(> 100 ${\mu}g/ml$). In addition, LPS increased NO production, iNOS expression and phosphorylation of $I{\kappa}-B{\alpha}$, which were blocked by the treatment of SML ether fraction in a dose dependent manner. Furthermore, the treatment of LPS increased TNF-${\alpha}$ production. However, the pretreatment of SML ether fraction prevented the LPS-induced TNF-${\alpha}$ production in dose dependant manner. Taken together, our results suggest that SML may be a beneficial drug against inflammatory diseases such as sepsis.

• Korean Journal of Food Science and Technology
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• v.38 no.6
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• pp.829-834
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• 2006

LP-BM5 murine leukemia retrovirus induces the immune dysfunction by imbalanced secretion of Th1 and Th2 cytokines in the murine AIDS model. In the present study, it was investigated whether pycnogenol (Pyc) administration could deactivate $NF-{\kappa}B$ to regulate the gene expression of Th1 and Th2 cytokines in C57BL/6 mice with murine AIDS. Treatment with Pyc for 12 weeks significantly inhibited the loss of body weight and enlargement of spleen and lymph node usually seen with AIDS. Moreover, Pyc increased the plasma level of Th1 cytokines, IL-2 and $IFN-{\gamma}$, while reducing the plasma level of Th2 cytokines, IL-6, IL-10, and $TNF-{\alpha}$. In primary culture of splenocytes, mRNA expression of Th2 cytokines was suppressed, but that of Th1 cytokines was not affected. The LP-BM5 retrovirus infection stimulated the cytoplasmic activation of $NF-{\kappa}B$ and nuclear translocation of $I-{\kappa}B$, whereas Pyc administration significantly reduced $NF-{\kappa}B$ activation and $I-{\kappa}B$ degradation. These results suggested that the inhibitory effect of Pyc on Th2 cytokines in mice with murine AIDS was dependent on suppression of the $NF-{\kappa}B$ signaling pathway and was not dependent on $INF-{\gamma}$ level, which regulates Th2 cytokines.