• Journal of the Society of Cosmetic Scientists of Korea
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• v.32 no.3 s.58
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• pp.173-180
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• 2006

Sesame (Sesamum indicum L.), one of the oldest oilseed crops, has been known to posses antioxidative and inflammatory effects. This seed contains lignan compounds such as sesamin, sesamol, sesaminol, sesaminol diglucosides (SDG), and sesaminol triglucosides (STG). Sesamin, a major lignan in sesame, displayed several biological activities including a protective effects against oxidative damage in the skin. In the present study, we investigated the effect of sesamin, sesamol, sesaminol, SDG, and STG, on nitric oxide (NO) induction and inducible nitric oxide synthane (iNOS) and cyclooxygenases-2 (COX-2) expression in lipopolysaccharides (LPS)-treated RAW 264.7 cells. The results showed that sesamol and sesaminol significantly inhibited NO generation but they were also cytotoxicity however, sesamin effectively inhibited NO production ($IC_{50}: 64{\mu}M$) without my cytotoxic effect in LPS-stimulated macrophage RAW 264.7 cells. In further study, it was founded that sesamin inhibited the expression of inducible nitric oxide synthase but not COX-2 expression. These results suggest that sesamin may be useful for improvements of the inflammatory diseases.

• Journal of Pharmacopuncture
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• v.5 no.2
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• pp.40-51
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• 2002

Objectives : The purpose of this study was to investigate the effect of Bee Venom on the lipopolysaccharide-induced expression phospholipase $A_2$, cyclooxygenase-2 and inducible nitrogen oxide synthase, and the generation of arachidonic acid, prostaglandin D2 and E2 in RAW 264.7 cells, a murine macrophage cell line. Methods : The expression of phospholipase $A_2$, cyclooxygenase and inducible nitrogen oxide synthase was determined by western blotting with corresponding antibodies, and the generation of arachidonic acid, prostaglandin $D_2$ and $E_2$ was assayed by ELISA method in RAW 264.7 cells. The non-toxic concentrations (0.1 to $5\;{\mu}g/ml$) of bee venom determined by MTT assay, were used in this study. Results : 1. Bee venom inhibited lipopolysaccharide-induced expression of phospholipase $A_2$ in a dose dependent manner after 48 hours treatment. 2. Bee venom inhibited lipopolysaccharide-induced expression of cyclooxygenase-2 in a dose dependent manner after 24 and 48 hours treatment. 3. Bee venom inhibited lipopolysaccharide-induced expression of inducible nitrogen oxidesynthase in a dose dependent manner after 48 hours treatment. 4. The generation of arachidonic acid, prostaglandin $D_2$ and $E_2$ was not much affected by the treatment of bee venom on the lipopolysaccharide-induced generation of arachidonic acid, prostaglandin $D_2$ and $E_2$ in RAW 264.7 cells.

• Journal of Life Science
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• v.33 no.1
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• pp.50-55
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• 2023

This study was designed to determine the activities of Rosa davurica Pall. leaf extract and their regulatory mechanisms in macrophage inflammation. Anti-inflammatory potential of Rosa davurica Pall. leaf extract was evaluated by measuring the nitric oxide (NO) release and inducible nitric oxide synthase (iNOS) synthesis in lipopolysaccharide (LPS)-treated macrophage Raw 264.7 cells. Rosa davurica Pall. leaf extract potently inhibited LPS-induced NO release in a dose dependent manner. However, cell viability decreased to about 50% at high dose of 500 ㎍/ml, resulting in cytotoxicity. LPS-induced iNOS protein expression was also reduced significantly after treatment with Rosa davurica Pall. leaf extract. Furthermore, extract of Rosa davurica Pall. attenuated LPS-mediated phosphorylation of IκB and nuclear factor (NF-κB). Suppression of NF-κB signaling by treatment with PDTC, an NF-κB specific inhibitor, accelerated the inhibition of NO production and iNOS protein expression. These results suggest that Rosa davurica Pall. exhibits the anti-inflammatory potential in LPS-induced macrophage inflammation, partly through inhibition of NO production by down-regulation of NF-κB signaling.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.130-130
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• 2001

Silymarin, a polyphenolic flavonoid antiodant, has been shown to have anti-inflammatory, hepatoprotective, and anticarcinogenic effects. In the present study, we report the inhibitory effect of silymarin on nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) mRNA expression in macrophages. In vivo administration of silymarin attenuated NO production of peritoneal macrophages in lipopolysaccharide (LPS)-treated mice.(omitted)

• Journal of Acupuncture Research
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• v.22 no.2
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• pp.111-121
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• 2005

Human placental extract (HPE), which is prepared from the placenta of healthy pregnant females, has been widely used in clinical field. HPE is known to possess anti-inflammatory, anti-viral, anti-oxidative, anti-mutagenic, and analgesic properties. In this study, the effect of HPE against lipopolysaccharide (LPS)-induced inflammation was investigated. From the present results, HPE was shown to suppress prostaglandin E2 synthesis (PGE2) and nitric oxide (NO) production by inhibition on the LPS-stimulated enhancement of the cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions in mouse BV2 microglial cells. These results suggest that HPE may offer a valuable mean of therapy for the treatment of brain inflammatory diseases by attenuating LPS-induced PGE2 and NO production.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.5
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• pp.515-521
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• 1997

Endothelial cells play a central role in the inflammatory processes, and activation of nuclear factor kappa B ($NF-_{\kappa}B$) is a key component in that inflammatory processes. Previously, we reported that tumor necrosis factor alpha($TNF{\alpha}$) had protective effect of cell death induced by serum deprivation and this protection was related to $NF-_{\kappa}B$ activation. Inducible nitric oxide synthase (iNOS) is a member of the molecules which transcription is regulated mainly by $NF-_{\kappa}B$. And the role of nitric oxide (NO) generated by iNOS on cell viability is still controversial. To elucidate the mechanism of $TNF{\alpha}$ and $NF-_{\kappa}B$ activation on cell death protection, we investigate the effect of NO on the cell death induced by serum- deprivation in bovine cerebral endothelial cells in this study. Addition of $TNF{\alpha}$, which are inducer of iNOS, prevented serum-deprivation induced cell death. Increased expression of iNOS was confirmed indirectly by nitrite measurement. When selective iNOS inhibitors were treated, the protective effect of $TNF{\alpha}$ on cell death was partially blocked, suggesting that iNOS expression was involved in controlling cell death. Exogenously added NO substrate (L-arginine) and NO donors (sodium nitroprusside and S-nitroso-N-acetylpenicillamine) also inhibited the cell death induced by serum deprivation. These results suggest that NO has protective effect on bovine cerebral endothelial cell death induced by serum-deprivation and that iNOS is one of the possible target molecules by which $NF-_{\kappa}B$ exerts its cytoprotective effect.

• BMB Reports
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• v.40 no.5
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• pp.636-643
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• 2007

This study was designed to identify and characterize the mechanism of macrophage activation by AAP, an acidic polysaccharide fraction isolated from the roots of Angelica sinensis (Oliv.) Diels. As a result, AAP significantly enhanced nitric oxide (NO) production and cellular lysosomal enzyme activity in murine peritoneal macrophages in vitro and in vivo. Furthermore, L-NAME, a specific inhibitor of inducible nitric oxide synthase (iNOS), effectively suppressed AAP-induced NO generation in macrophages, indicating that AAP stimulated macrophages to produce NO through the induction of iNOS gene expression and the result was further confirmed by the experiment of the increase of AAP-induced iNOS transcription in a dose-dependent manner. To further investigate, AAP was shown to strongly augment toll-like receptor 4 (TLR4) mRNA expression and the pretreatment of macrophages with anti-TLR4 antibody significantly blocked AAP-induced NO release and the increase of iNOS activity, and tumor necrosis factor-$\alpha$ (TNF-$\alpha$) secretion.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.3
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• pp.724-729
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• 2006

Many traditional herbal remedies exhibit several beneficial effects including anti-inflammation. The exact mechanism of the a-inflammato action of Panax notoginseng Buck F.H. Chen. however, has not been determined. In the present study, we have isolted the acting compound, emodin, from P. notoginseng and examined the effects of p. notoginseng and emodin on lipopolysaccharide (LPS)-induced nitric oxide (NO) production, and inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) gene expression in RAW264.7 macrophages. The results indicated that p. notoginseng concentration-dependently inhibited LPS-induced NO production. Furthermore, P. notoginseng inhibited the expression of LPS-induced iNOS and COX-2 proteins without an appreciable cytotoxic effect on RAW264.7 cells. Emodin also inhibited LPS-induced iNOS protein as potently as P. notoginseng. This was consistent with the findings that P. notoginseng but not emodin inhibited prostaglandin E2 synthesis induced Dy LPS.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.5
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• pp.1327-1333
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• 2006

Many traditional herbal remedies exhibit several beneficial effects including anti-inflammation. Panax notoginseng Buck F.H. Chen. is used as a therapeutic agent to stop haemorrhages and a tonic to promote health in Korean and Chinese medicine. The pharrnacokinetic profiles of the main P. notoginseng are still not accurately investigated. The exact mechanism of the anti-inflammatory action of P. notoginseng, however, has not been determined. In the present study, we examined the effect of P. notoginseng on lipopolysaccharide (LPS)-induced nitric oxide (NO) production, and inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) gene expression in RAW264.7 macrophages. The results indicated that P. notoginseng concentration-dependently inhibited LPS-induced NO production. Furthermore, P. notoginseng inhibited the expression of LPS-induced iNOS and COX-2 proteins without an appreciable cytotoxic effect on RAW264.7 cells. Berberine also inhibited LPS-induced iNOS protein as potently as P. notoginseng. This was consistent with the findings that P. notoginseng and also berberine inhibited prostaglandin E2 synthesis induced by LPS.

• Biomolecules & Therapeutics
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• v.16 no.3
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• pp.231-236
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• 2008

The current work was designed to assess novel pharmacological activities of 4-hydroxybenzaldehyde (HD), a major phenolic constituent of various natural products of plant origin, such as Gastrodia elata Blume. HD exhibited a significant inhibition in the chick chorioallantoic membrane (CAM) angiogenesis. HD also displayed an inhibitory effect in acetic acid-induced permeability in mice. Anti-nociceptive activity of HD was convinced using the acetic acid-induced writhing test in mice. HD was able to suppress production of nitric oxide (NO) and induction of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the lipopolysaccharide (LPS)-activated RAW264.7 macrophages. HD also diminished the reactive oxygen species (ROS) level elevated in the LPS-activated macrophages. In brief, HD exhibits anti-angiogenic, anti-inflammatory and anti-nociceptive activities possibly via down-regulating iNOS and/or COX-2, which may be partly responsible for pharmacological efficacies of various natural products.