• Title/Summary/Keyword: iNOS(inducible nitric oxide synthase)

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Effects of Dietary Intervention and Simvastatin on Plasma Nitric Oxide in Patients with Hyperlipidemia

  • Yim, Jungeun;Choue, Ryowon;Park, Changshin;Cha, Youngnam;Chyun, Jonghee
    • Nutritional Sciences
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    • v.7 no.4
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    • pp.214-217
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    • 2004
  • Dietary intervention and simvastatin is beneficial in the prevention cardiovascular diseases by lowering plasma lipid levels. Endothelial dysfunction is associated with coronary artery disease and its risk factors and is reversed by dietary intervention. It has been suggested that hyperlipidemia contributes to the development of atherosclerosis by increasing inducible nitric oxide synthase (iNOS) expression via intimal thickening. Statins treatment has been found to decrease iNOS expression and atherogenensis in animal models. We hypothesized that dietary intervention and simvastatin therapy could decrease plasma nitric oxide in hypercholesterolemic patients, which would suggest the opportunity for modulation of iNOS expression through the use of statins in a clinical situation. We measured the plasma levels of nitrite and nitrate (NOx) in 19 hyperlipidemia patients. The subjects were under dietary intervention following simvastatin therapy for 12 weeks. As a result, the plasma level of NOx, stable metabolites of nitric oxide (NO), saw a two-fold elevation in hyperlipidemic patients as compared to normal levels. Although 12 weeks of dietary intervention did not lower NOx levels, subsequent 12-week simvastatin (10 mg/day) treatment, along with dietary intervention, lowered NOx levels significantly. This NOx reduction, induced by simvastatin therapy, positively correlated with lowered coronary risk factors (r=0.40, p=0.02). It indicated that simvastatin therapy decreases plasma NOx levels by, perhaps, decreasing iNOS expression or activity leading to the attenuation of the development of neointima.

Effects of Astaxanthin on the Production of NO and the Expression of COX-2 and iNOS in LPS-Stimulated BV2 Microglial Cells

  • Choi, Seok-Keun;Park, Young-Sam;Choi, Dong-Kug;Chang, Hyo-Ihl
    • Journal of Microbiology and Biotechnology
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    • v.18 no.12
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    • pp.1990-1996
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    • 2008
  • Astaxanthin has shown antioxidant, antitumor, and anti-inflammatory activities; however, its molecular action and mechanism in the nervous system have yet to be elucidated. We examined the in vitro effects of astaxanthin on the production of nitric oxide (NO), as well as the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. Astaxanthin inhibited the expression or formation of nitric oxide (NO), iNOS and COX-2 in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Astaxanthin also suppressed the protein levels of iNOS and COX-2 in LPS-stimulated BV2 microglial cells. These results suggest that astaxanthin, probably due to its antioxidant activity, inhibits the production of inflammatory mediators by blocking iNOS and COX-2 activation or by the suppression of iNOS and COX-2 degradation.

Tribulus terrestris Suppresses the Lipopolysaccharide-Induced Inflammatory Reaction in RAW264.7 Macrophages through Heme Oxygenase-1 Expressions

  • Kim, Jai Eun
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.28 no.1
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    • pp.63-68
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    • 2014
  • The fruit of Tribulus terrestris L. (Zygophyllaceae) is an important source of traditional Korean and Chinese medicines. In this study, NNMBS223, consisting of the ethanol extract of T. terrestris, showed potent anti-inflammatory activities in RAW264.7 macrophages. We investigated the effect of NNMBS223 in suppressing the protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and production of iNOS-derived nitric oxide (NO), COX-2-derived prostaglandin E2 (PGE2) in lipopolysaccharide (LPS)-stimulated macrophages. In addition, NNMBS223 induced expression of heme oxygenase (HO)-1 through nuclear translocation of nuclear factor E2-related factor 2 (Nrf2) in macrophages. The effects of NNMBS223 on LPS-induced production of NO and PGE2 were partially reversed by the HO activity inhibitor tin protoporphyrin (SnPP). These findings suggest that Nrf2-dependent increases in expression of HO-1 induced by NNMBS223 conferred anti-inflammatory activities in LPS stimulated RAW264.7 macrophages.

Anti-Inflammatory Effect of Extracts from Ligustrum obtusifolium S. fruits in RAW 264.7 Macrophages (RAW 264.7 대식세포 내에서 남정목 열매 추출물의 항염증 효과)

  • Moon, Ju-Ho;Go, Heung;Shin, Seon-Mi;Kim, Ki-Tae
    • The Journal of the Society of Korean Medicine Diagnostics
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    • v.17 no.3
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    • pp.263-273
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    • 2013
  • Objectives This study was designed to investigate the anti-inflammatory effect of extracts from Ligustrum obtusifolium S. fruits(LOF) in RAW 264.7 Macrophages stimulated with lipopolysaccharide(LPS). Methods We examined productions of nitric oxide(NO), reactive oxygen species(ROS), inducible isoforms of NO synthase(iNOS), cyclooxygenase-2(COX-2) to investigate the anti-inflammatory effect of LOF extracts. In addition, we measured generation of pro-inflammatory cytokines(TNF-${\alpha}$, IL-6). Results Cell viability showed that LOF extracts had no cytotoxicity in Raw 264.7 cells. The treatment with LOF extracts significantly decreased the generation of NO and pro-inflammatory cytokines(TNF-${\alpha}$, IL-6) in LPS-stimulated macrophage cells. Furthermore LOF extracts inhibited intracellular ROS generation dose dependently and reduced the expression of iNOS, COX-2 proteins. Conclusions These results showed that the LOF extracts had an anti-inflammatory effect on LPS-stimulated Raw 264.7 cells. These findings provide scientific support for the use of this Ligustrum obtusifolium S. for inflammatory-related diseases.

Inhibitory effect of Yongdamsagantang water extract on IL-6 and nitric oxide production in lipopolysaccharide-activated RAW 264.7 cells

  • Lim, Jin-Ho;Lee, Jong-Rok;Kim, Sang-Chan;Jee, Seon-Young
    • Advances in Traditional Medicine
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    • v.7 no.3
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    • pp.321-329
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    • 2007
  • The present study was conducted to evaluate the effect of Yongdamsagantang (YST) on the regulatory mechanism of cytokines and nitric oxide (NO) for the immunological activities in RAW 264.7 cells. After the treatment of YST water extract, cell viability was measured by MTT assay, and NO production was monitored by measuring the nitrite content in culture medium. Inducible nitric oxide synthase (iNOS) and phospholylation of inhibitor of nuclear factor kappa B alpha ($p-I{\kappa}B{\alpha}$) were determined by Immunoblot analysis, and levels of cytokine were analyzed by sandwich immunoassays. Results provided evidences that YST inhibited the production of NO. iNOS, and interleukin-6, and the activation of $p-I{\kappa}B{\alpha}$ in RAW 264.7 cells activated with lipopolysaccharide. These findings showed that YST could have some anti-inflammatory effects which might play a role in therapy in Gram-negative bacterial infections.

Lead increases Nitric Oxide Production in Immunostimulated Glial Cells

  • Choi, Min-Sik;Shin, Chan-Young;Ryu, Jae-Ryun;Lee, Woo-Jong;Cheong, Jae-Hoon;Choi, Chang-Rak;Kim, Won-Ki;Ko, Kwang-Ho
    • Biomolecules & Therapeutics
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    • v.12 no.4
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    • pp.209-214
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    • 2004
  • Lead has long been considered as a toxic environmental pollutant that severely damages the central nervous system. In various neurogenerative diseases, actrocytes become activated by proinflammatory cytokines. In the present study, we investigated whether lead (Pb$^{2+}$) affects inducible nitric oxide synthase (iNOS) expression in activated glial cells. Rat primary glial cells were stimulated with lipopolysaccharide (LPS, 1 ${\mu}$g/ml) plus IFN$_{\gamma}$(100 U/ml). Pre-treatment of Pb$^{2+}$ increased nitric oxide (NO) production in LPS/IFN$_{\gamma}$-stimulated glial cells. Lead itself, however, suppressed the basal production of NO in control glial cells. Addition of the iNOS inhibitors L-NAME (1 mM) and L-NNA (800 ${\mu}$M) prevented the Pb$^{2+}$-induced increase in NO production. Western blot analysis showed that pre-treatment of Pb$^{2+}$ augmented LPS/IFN$_{\gamma}$-induced increase in iNOS immunoreactivity, which was well correlated with the increased NO production. In addition, pre-treatment of Pb$^{2+}$ synergistically increased the iNOS mRNA expression induced by LPS and IFN${\gamma}$. The present results indicate that lead intoxication adversely affect brain function by potentiating iNOS expression and NO production in activated glial cells observed in various neurodegenerative diseases.

Suppression Effect of Curcuma longa Rhizome-Derived Components against Nitric Oxide Synthase

  • Lee, Hoi-Seon
    • Journal of Applied Biological Chemistry
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    • v.52 no.4
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    • pp.212-215
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    • 2009
  • The inhibitory effects of Curcuma longa rhizome-derived materials against nitric oxide (NO) production were assessed. The inhibitory effect (57%) on NO production was evidenced by the methanol extract of C. longa at $1\;{\mu}g/mL$. In the fractionation of the methanol extract, the ethyl acetate fraction evidenced an inhibitory effect greater than 62.1% at $1\;{\mu}g/mL$. The active constituent was identified as curcumin. Curcumin exerted potent inhibitory effects of 78.7 and 65.7% at concentrations of 1 and $0.5\;{\mu}g/mL$, respectively. Furthermore, the inhibitory effect of ar-turmerone was measured as 31.3 and 15.8% at 1 and $0.5\;{\mu}g/mL$, respectively. The iNOS expression-suppressive effects of curcumin were assessed via western blot analysis. Our results suggest that curcumin and ar-turmerone may prove useful in the development of new types of NO inhibitors.

Anti-Oxidant and Antiinflammatory Effects of Rosa multiflora Root (찔레나무뿌리(Rosa multiflora root)의 항산화 및 항염증효과)

  • Park, Geun-Hye;Lee, Jin-Young;Kim, Dong-Hee;Cho, Young-Je;An, Bong-Jeun
    • Journal of Life Science
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    • v.21 no.8
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    • pp.1120-1126
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    • 2011
  • Rosa multiflora thunberg belonging to Rosaceae is widely distributed in East Asia including Korea and Japan, and has been reported to have tormentic acid and rosamultin. To develop a new natural anti-inflammatory agent for cosmetics, we investigated the inhibitory effects of inflammation in Rosa multiflora root (R. multiflora root). The biological activity and anti-inflammatory effects were investigated by water, ethanol, methanol and acetone extracts of R. multiflora root. The measurements of polyphenol content from R. multiflora root were highest in water and acetone extracts, at 57.48 ${\pm}$ 0.88 mg/g and 67.05 ${\pm}$ 0.56 mg/g, respectively. The result of DPPH, ABTS and superoxide anion radical scavenging effects showed over 50% efficacy at 50 ${\mu}g/ml$ in ethanol, methanol and acetone extracts. Hyaluronidase inhibition effect showed over 60% efficacy at 500 ${\mu}g/ml$ in ethanol, methanol, and acetone extracts. Nitric oxide radical inhibition effect of R. multiflora root ethanol extracts showed over 30% efficacy at 500 ${\mu}g/ml$. We investigated the effect of R. multiflora root extracts on nitric oxide (NO) production of inducible nitric oxide synthase (iNOS) in LPS-induced RAW 264.7 macrophage cells. The result showed that R. multiflora root extracts have an inhibitory effect on NO production and iNOS expression and also can be used as an anti-inflammatory agent. These antioxidant and anti-inflammatory effects of R. multiflora root show applicant potential application as a functional cosmetic material.

Anti-inflammatory Effect of Achyranthoside E Dimethyl Ester in LPS-stimulated RAW 264.7 Cells (LPS로 인한 RAW 264.7 세포의 염증반응에 미치는 achyranthoside E dimethyl ester의 효과)

  • Bang, Soo Young;Kim, Ji-Hee;Moon, Hyung-In;Kim, Young Hee
    • Journal of Life Science
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    • v.23 no.6
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    • pp.736-742
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    • 2013
  • Achyranthoside E dimethyl ester (AEDE) is an oleanolic acid glycoside from Achyranthes japonica. In this study, we investigated the effects of AEDE on nitric oxide (NO) production and underlying molecular mechanisms in lipopolysaccharide (LPS)-stimulated macrophages. AEDE inhibited LPS-induced NO secretion as well as inducible NO synthase (iNOS) expression, without affecting cell viability. Further study demonstrated that AEDE induced heme oxygenase-1 (HO-1) gene expression. In addition, the inhibitory effects of AEDE on iNOS expression were abrogated by small interfering RNA-mediated knock-down of HO-1. Moreover, AEDE induced nuclear translocation of nuclear factor E2-related factor 2 (Nrf2), a transcription factor that regulates HO-1 expression. AEDE-induced expression of HO-1 was inhibited by inhibitors of phosphatidylinositol 3-kinase (PI-3K) and extracellular signal regulated kinase (ERK1/2). AEDE phosphorylated Akt and ERK1/2 as well. Therefore, these results suggest that AEDE suppresses the production of pro-inflammatory mediator such as NO by inducing HO-1 expression via PI-3K/Akt/ERK-Nrf2 signaling. These findings provide the scientific rationale for anti-inflammatory therapeutic use of AEDE.

Extracts of Artemisia princeps Pampanini Inhibit Lipopolysaccharide-induced Nitric Oxide, Cyclooxygenase-2, Prostaglandin $E_2$, and Tumor Necrosis Factor-$\alpha$ Production from Murine Macrophage RAW 264.7 Cells (강화사자발쑥의 마크로파지 RAW 264.7세포에 대한 Tumor Necrosis Factor-$\alpha$, Prostaglandin $E_2$, Cyclooxygenase-2 및 LPS 유도 Nitric Oxide 생성 저해)

  • Yun, Jun-Yong;Choi, Se-Yong;Park, Pyo-Jam;Chung, Hae-Gon;Shin, Heung-Mook;Suk, Kyoung-Ho;Lim, Beong-Ou
    • Korean Journal of Medicinal Crop Science
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    • v.16 no.5
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    • pp.326-331
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    • 2008
  • To search for immunoactive natural products exerting anti-inflammatory activity, we have evaluated the effects on the water extracts of Artemisia princeps Pampanini (APP) on lipopolysaccharide-induced nitric oxide (NO), tumor necrosis factor-$\alpha$ (TNF-$\alpha$), and prostaglandin $E_2$ ($PGE_2$) production by RAW 264.7 macrophage cell line. Our data indicate that this extract is a potent inhibitor of NO production and it also significantly decreased PGE2 and TNF-$\alpha$ production. Consistent with these results, the protein and mRNA expression level of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) was inhibited by water extracts of APP in a dose-dependent manner. These results suggest that APP may exert anti-inflammatory and analgesic effects possibly by suppressing the inducible NO synthase and COX-2 expressions.