• Tuberculosis and Respiratory Diseases
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• v.60 no.4
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• pp.426-436
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• 2006

Background : Particulate matters (PM) when inhaled is known to induce pulmonary diseases including asthma and chronic bronchitis when inhaled. Despite the epidemiological proofevidence, the pathogenesis of PM-related pulmonary diseases is unclearremain poorly understood. Methods : Primary alveolar macrophages were harvested from the SPF and inflammatory rats by bronchioalveolar lavage (BAL). The cultured primary alveolar macrophages were treated with the medium only, PM only ($5{\sim}40{\mu}g/cm^2$), LPS (5ng/ml) only, and PM with LPS for 24 and 48 hours. The level of secreted nitric oxide (NO) was assayed from the cultured medium by using the Griess reaction. The cultured cells were utilized for the western blotting against the inducible nitric oxide synthase (iNOS) proteins. Immunocyto- chemical staining against the iNOS and NT-proteins were performed in cells that cultured in the $Lab-Tek^{(R)}$ chamber slide after treatments. Results : The PM that utilizein this experiments induced NO formation with iNOS expression in the cultured SPF and inflammatory rats alveolar macrophages, by itself. When the cells were co-treated with PM and LPS, there was a statistically significant synergistic effect on NO formation and iNOS expression over the LPS effect. The cells from the sham control showed minimal immunoreactivity for the NT-proteins. Significantly higher quantities of NT-proteins were detected in the PM and PM with LPS co-treated cells than from the sham control. Conclusion : Increased iNOS expression and NO formation with increased NT-proteins formation might be involved in the pathogenesis of PM-induced lung injury.

• Journal of Applied Biological Chemistry
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• v.56 no.4
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• pp.249-255
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• 2013

Recently, algae has been considered as a potential anti-inflammatory source due to its distinctive habitat environment exposing to light and high oxygen concentration. In present study, anti-inflammatory effect of brown alga, Sargassum fullvellum ethanol extract (SFEE), was examined. SFEE inhibited not only the production of nitric oxide and pro-inflammatory cytokines (IL-6, IL-$1{\beta}$, TNF-${\alpha}$) but also the expression of inducible nitric oxide synthase and cyclooxygenase 2 in LPS-induced RAW 264.7 cells without affecting cell viability. SFEE also suppressed the expression of nuclear factor kappa B (NF-${\kappa}B$), suggesting that SFEE could affect the expression of inflammation related cytokines and proteins through the regulation of NF-${\kappa}B$. Furthermore, formation of edema of the ear was 40% lower in mice treated with the highest dose (250 mg/kg) of SFEE than in the control mice. Thus, our study showed that SFEE may be a potential therapeutic anti-inflammatory drug.

• 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.

• Toxicological Research
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• v.13 no.3
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• pp.247-250
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• 1997

We have studied cytotoxicity of S-nitroso-N-acetyl- N-DL-penicillamine(SNAP), a Nitric oxide (NO)-releasing compound, in RAW264.7 macrophages. SNAP is cytotoxic to RAW264.7 cells in a concentration-dependent manner. PMA(200 nM) stimulated cells to produce superoxide anton radical($O_2^{-\cdot}$) and caused a little loss of RAW264.7 cell viability for 12 hr and diminished the cytotoxicity of SNAP. The mechanism by which PMA can protect cells against NO-mediated cytotoxicity was studied by peroxynitrite-enhanced chemiluminescence method. Observed results suggested that $O_2^{-\cdot}$ produced by PMAstimulated RAW264.7 cells may quench NO released by SNAP and reduce NO, thus attenuating NO-related damages.

• Plant Biotechnology Reports
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• v.4 no.4
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• pp.243-251
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• 2010

Nitric oxide (NO) has been shown to be involved in diverse physiological processes in microbes, animals and plants. In this study, the involvement of NO in the development and possible roles in oxidative stress protection of Chinese cabbage (Brassica rapa subsp. pekinensis cv. Samrack-ulgari) seedlings were investigated. Exogenous application of sodium nitroprusside (SNP) retarded root elongation, while increasing lateral root formation of Chinese cabbage. Plants showed no signs of external stress due to SNP application in true leaves. Cotyledons of 3-week-old Chinese cabbage plants were found to be highly sensitive to SNP application. Treated cotyledons displayed rapid tissue collapse and associated cell death. Although SNP application reduced root growth under normal growth conditions, it also enhanced methyl viologen (MV)-mediated oxidative stress tolerance. Analysis of SNP application to Chinese cabbage leaf disks, revealed SNP-induced tolerance against oxidative stresses by MV and $H_2O_2$, and evidence includes prevention of chlorophyll loss, superoxide anion (${O_2}^-$) accumulation and lipid peroxidation. This report supports a role for nitric oxide in modulating early seedling development, programmed cell death and stress tolerance in Chinese cabbage.

• Journal of the Korean Electrochemical Society
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• v.5 no.4
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• pp.209-211
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• 2002

The simultaneous sensing of nitric oxide (NO) and its metabolite, nitrite $(NO_2^-)$ has been studied by Osteryoung square-wave voltarnmetery (OSWV) in physiological pH solution (0.1 M phosphate buffer solution, pH 7.2). Using an electrochemically pretreated glassy carbon (GC) electrode, OSWV was successfully applied to observe the well-separated oxidation peaks at ca. 0.58 and 0.80V vs. Ag/AgCI for NO and $(NO_2^-)$, respectively. This clear separation between the NO and $(NO_2^-)$ oxidation peaks may be due to the formation of surface oxides (e.g., quinone (C=O) or carboxylic $(COO^-)$ group) and surface defects introduced by the electrochemical pretreatment of GC electrodes.

• Journal of Ginseng Research
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• v.32 no.2
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• pp.89-98
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• 2008

There are increasing evidences in the literatures on the potential role of ginsenosides in treating cardiovascular diseases. In this article, current information about ginsenosides-mediated vascular relaxation are reviewed. From the published studies using isolated organs, cell culture systems and animal models, ginsenosides are shown to relax blood vessels and improve blood flow through diverse mechanisms, including nitric oxide release by activating eNOS phosphorylation via PI3K/Akt and/or ERK1/2 pathways in endothelial cells, induction of inducible nitric oxide synthase through activation of NF-${\kappa}$B, reducing the intracelluar Ca$^{2+}$ levels by activating Ca$^{2+}$-activated K$^{+}$ channels in vascular smooth muscle cells and reducing platelet aggregation by decreasing thromboxane A$_2$ formation and intracelluar Ca$^{2+}$in platelets. In addition, the relevant clinical trials regarding the effects of ginsenosides on the cardiovascular disease are summarized, particulary focusing on managing hypertension and improving thrombotic disorders. Finally, antagonistic effects of ginsenosides on the prostaglandin H$_2$ receptor and scavenging effects on the generation of oxygen-derived free radicals in spontaneously hypertensive rats (SHR) are discussed.

• Nutrition Research and Practice
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• v.9 no.2
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• pp.123-128
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• 2015

BACKGROUND/OBJECTIVES: Natural products or active components with a protective effect against oxidative stress have attracted significant attention for prevention and treatment of degenerative disease. Oligonol is a low molecular weight polyphenol containing catechin-type monomers and oligomers derived from Litchi chinensis Sonn. We investigated the protective effect and its related mechanism of oligonol against oxidative stress. MATERIALS/METHODS: Oxidative stress in C6 glial cells was induced by hydrogen peroxide ($H_2O_2$) and the protective effects of oligonol on cell viability, nitric oxide (NO) and reactive oxygen species (ROS) synthesis, and mRNA expression related to oxidative stress were determined. RESULTS: Treatment with oligonol inhibited NO and ROS formation under cellular oxidative stress in C6 glial cells. In addition, it recovered cell viability in a dose dependent-manner. Treatment with oligonol also resulted in down-regulated mRNA expression related to oxidative stress, nuclear factor kappa-B (NF-${\kappa}B$) p65, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), compared with the control group treated with $H_2O_2$. In particular, expression of NF-${\kappa}B$ p65, COX-2, and iNOS was effectively reduced to the normal level by treatment with $10{\mu}g/mL$ and $25{\mu}g/mL$ of oligonol. CONCLUSIONS: These results indicate that oligonol has protective activity against oxidative stress-induced inflammation. Oligonol might be a promising agent for treatment of degenerative diseases through inhibition of ROS formation and NF-${\kappa}B$ pathway gene expression.

• Tuberculosis and Respiratory Diseases
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• v.42 no.4
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• pp.447-454
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• 1995

Cytokine release from alveolar macrophages and subsequent interaction of these cytokines with the bronchial epithelium can induce epithelial cells to release inflammatory mediators. Nitric oxide(NO), a highly reactive gas formed from arginine by nitric oxide synthase(NOS), is known to be involved in inflammation and edema formation, and the inducible form of NOS(iNOS) can be increased by cytokines. In this context, we hypothesized that lung epithelial cells could be stimulated by cytokines released by alveolar macrophages to express iNOS. To test this hypothesis, the murine lung epithelial cell line, LA-4, or the human lung epithelial cell line, A549, were stimulated with culture supernatant fluids from alveolar macrophages. NO production was assessed by evaluating the culture supernatant fluids for nitrite and nitrate, the stable end products of NO. Both murine and human cell culture supernatant fluids demonstrated an increase in nitrite and nitrate which were time- and dose-dependent and attenuated by $TNF{\alpha}$ and IL-$1{\beta}$ antibodies(p<0.05, all comparisons). Consistent with these observations, cytomix a combination of $TNF{\alpha}$, IL-$1{\beta}$, and $\gamma$-interferon, stimulated the lung epithelial cell lines as well as primary cultures of human bronchial epithelial cells to increase their NO production as evidenced by an increase in nitrite and nitrate in their culture supernatant fluids, an increase in the iNOS staining by immunocytochemistry, and an increase in iNOS mRNA by Northern blottin(p<0.05, all comparisons). The cytokine effects on iNOS were all attenuated by dexamethasone. To determine if these in vitro observations are reflected in vivo, exhaled NO was measured and found to be increased in asthmatics not receiving corticosteroids. These data demonstrate that alveolar macrophage derived cytokines increase iNOS expression in lung epithelial cells and that these in vitro observations are mirrored by increased exhaled NO levels in asthmatics. Increased NO in the lung may contribute to edema formation and airway narrowing.

• Journal of Plant Biotechnology
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• v.34 no.3
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• pp.213-221
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• 2007

The treatment of radish cotyledons with a nitric oxide (NO)-releasing substance, sodium nitroprusside (SNP) resulted in an increased adventitious root development in a dose-dependent manner. However, this NO-mediated enhancement effect was reversed when either 0.5 mM EGTA (an extracellular $Ca^{2+}$ chelator) or 0.1 mM $LaCl_3$ (a calcium channel blocker) was applied with $50\;{\mu}M$ SNP. Our results also showed that guaiacol peroxidase (GPX) and syringaldazine peroxidase (SPX) activities, which are known to play a key role in rooting, were more largely increased during adventitious root induction in the cotyledons treated with SNP. However, the treatment of cotyledons with SNP plus $LaCl_3$ inhibited the SNP-induced increases in the activities of both GPX and SPX. Trifluoperazine (TFP), an antagonist of calmodulin (a specific calcium-binding protein), also delayed adventitious root formation and significantly reduced the root length and number of the SNP-treated cotyledons as well as the deactivation of GPX and SPX enzymes. In conclusion, our results suggest that calcium is involved in the NO response leading to induction of adventitious root through a regulation of GPX and SPX.