• 대한화장품학회지
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• 제41권1호
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• pp.45-55
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• 2015

자외선은 외부적인 스트레스 자극인자로 작용하여 사람 각질형성세포에서 reactive oxygen species (ROS)와 비활성 코르티손을 활성 코르티솔로 전환시키는 효소인 $11{\beta}$-hydroxysteroid dehydrogenase type 1 ($11{\beta}$-HSD1)의 발현 및 활성을 증가시킨다고 알려져 있다. 또한, ROS가 증가된 피부에서는 염증 유발 사이토카인과 염증 매개 인자의 발현이 증가되어 결과적으로 염증반응을 일으키게 되는 원인이 된다. 본 연구에서는 각질형성세포(HaCaT)에서 $11{\beta}$-HSD1 억제제가 ROS 분해효소인 catalase의 생성을 회복시킴에 착안하여, $11{\beta}$-HSD1의 발현을 저해함과 동시에 ROS로부터 유도되는 염증 반응을 억제하는 천연물 소재를 발굴하고자 하였다. 그 중 능실 추출물과 그 분획물은 각각 $11{\beta}$-HSD1의 발현과 ROS 생성 증가를 억제하고, 염증성 사이토카인인 tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\alpha}$, $-1{\beta}$의 발현을 억제하였다. 또한, 자외선에 의해 유도되는 염증 매개인자인 cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS), prostaglandin $E_2$ ($PGE_2$)의 생성을 저해하였다. 따라서 본 연구 결과로부터 능실 추출물 및 그 분획물은 $11{\beta}$-HSD1의 발현을 억제함과 동시에 ROS에 의해 유발된 피부 염증 반응을 효과적으로 저해함을 확인하였다.

• 대한의생명과학회지
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• 제18권4호
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• pp.338-344
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• 2012

Mollugin is the active compound of Rubia cordifolia, a well known herb widely used in alternative medicines for the treatment of various inflammatory diseases including arthritis and uteritis. In the present study, we investigated the anti-inflammatory effects of mollugin in lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophage cells. Treatment with mollugin significantly inhibited LPS-induced release of nitric oxide, prostaglandin $E_2$, and inflammatory cytokines, such as tumor necrosis factor-${\alpha}$ and interleukin-6. In addition, mollugin suppressed LPS-induced nuclear factor-kappa B (NF-${\kappa}B$) transcriptional activity. These results suggest that mollugin inhibits LPS-induced expression of inflammatory molecules via NF-${\kappa}B$, at least in part, and indicate the potential value of mollugin as a valuable new drug candidate for the treatment of various inflammatory diseases.

• 동의생리병리학회지
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• 제34권5호
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• pp.238-244
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• 2020

Yangdan-tang (YD) is recorded as a treatment to treat exterior-related fever illness in the Korean medicine. In this study, we examined the anti-inflammatory effects of YD, using YD water extract and lipopolysaccharide (LPS)-induced RAW 264.7 cells. First of all, we measured the amount of nitric oxide (NO) and prostaglandin E2 (PGE2), the products of inflammatory metabolism. Also, we measured enzymes such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as cytokines such as tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 1 alpha (IL-1α), and interleukin 1 beta (IL-1β). YD suppressed the production of NO and PGE2 in a dose dependent manner and reduced the amount of protein and the mRNA expression of iNOS and COX-2. Also, YD reduced the mRNA expression of TNF-α, IL-6, IL-1α and IL-1β. In conclusion, YD decreased production of LPS-induced inflammatory factor, which could be a clinical basic subject for inflammatory diseases.

• Nutrition Research and Practice
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• 제11권2호
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• pp.90-96
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• 2017

BACKGROUND/OBJECTIVES: Although the antioxidative effects of lycopene are generally known, the molecular mechanisms underlying the anti-inflammatory properties of lycopene are not fully elucidated. This study aimed to examine the role and mechanism of lycopene as an inhibitor of inflammation. METHODS/MATERIALS: Lipopolysaccharide (LPS)-stimulated SW 480 human colorectal cancer cells were treated with 0, 10, 20, and $30{\mu}M$ lycopene. The MTT assay was performed to determine the effects of lycopene on cell proliferation. Western blotting was performed to observe the expression of inflammation-related proteins, including nuclear factor-kappa B ($NF-{\kappa}B$), inhibitor kappa B ($I{\kappa}B$), mitogen-activated protein kinase (MAPK), extracellular signal-related kinase (ERK), c-jun NH2-terminal kinase (JNK), and p38 (p38 MAP kinase). Real-time polymerase chain reaction was performed to investigate the mRNA expression of tumor necrosis factor ${\alpha}$ ($TNF-{\alpha}$), interleukin-1 beta ($IL-1{\beta}$), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Concentrations of nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) were determined via enzyme-linked immunosorbent assays. RESULTS: In cells treated with lycopene and LPS, the mRNA expression of $TNF-{\alpha}$, $IL-1{\beta}$, IL-6, iNOS, and COX-2 were decreased significantly in a dose-dependent manner (P < 0.05). The concentrations of $PGE_2$ and NO decreased according to the lycopene concentration (P < 0.05). The protein expressions of $NF-{\kappa}B$ and JNK were decreased significantly according to lycopene concertation (P < 0.05). CONCLUSIONS: Lycopene restrains $NF-{\kappa}B$ and JNK activation, which causes inflammation, and suppresses the expression of $TNF-{\alpha}$, $IL-1{\beta}$, IL-6, COX-2, and iNOS in SW480 human colorectal cancer cells.

• 생약학회지
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• 제34권3호통권134호
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• pp.223-227
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• 2003

In the present study, anti-inflammatory activity of amygdalin isolated from persicae Semen have been evaluated on lipopolysaccharide (LPS)-induced release of nitric oxide (NO), prostaglandin $E_2\;(PGE_2)$ and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) by the macrophage RAW 264.7 cells. Amygdalin significantly inhibited generation of NO and $TNF-{\alpha}$ on LPS-stimulated RAW264.7 cells in a concentration-dependent manner. Consistent with these observations, the expression of inducible NO synthase (iNOS) enzyme was also inhibited by amygdalin in a concentration-dependent manner. However, amygdalin did not show any influence on the synthesis of $PGE_2$ and the expression of COX-2. Thus, this study suggests that amygdalin-mediated inhibition of iNOS expression, and $TNF-{\alpha}$ release may be one of the mechanisms responsible for the anti-inflammatory effects of Persicae Semen.

• Natural Product Sciences
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• 제20권1호
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• pp.51-57
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• 2014

In this study, the anti-inflammatory effects of ethanol extract of Rumex crispus L. and its fractions were investigated in RAW 264.7 macrophages. To evaluate the anti-inflammatory effects of extract, we studied nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), and tumor necrosis factor-alpha ($TNF-{\alpha}$) levels in RAW 264.7 cells. The ethanol extract of R. crispus L. significantly decreased NO production and the levels of other inflammatory factors, such as PGE2 and $TNF-{\alpha}$, in lipopolysaccharide (LPS)-stimulated macrophages in a dose-dependent manner. We also assessed the inducible nitric oxide synthase (iNOS) and the cyclooxygenase 2 (COX-2) protein expression by western blot. Ethyl acetate fraction of R. crispus L. had the strongest anti-inflammatory effect. These results suggest that ethyl acetate extract of R. crispus L. might be beneficial in the treatment of chronic inflammatory diseases.

• 약학회지
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• 제44권5호
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• pp.448-454
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• 2000

Microglia, brain resident macrophages, play a central role in the inflammatory responses of the brain and are activated in brain injuries and several neurodegenerative diseases such as Alzheimer's and Parkinson's disease, thereby aggravating the course of these diseases. In this study, the effects of plantderived compounds such as curcumin or gingerol on the microglial activation were examined. Microglial cultures were prepared from 2~3 week mixed primary glial cultures obtained from the cerebral cortex of 1~2 day old rats and identified by immunocytochemistry using microglial-specific antibody OX-42. Microglia were activated by lipopolysaccharide (LPS) and interferon-${\gamma}$ (IFN-${\gamma}$) and the effect of curcumin or 6-gingerol on the microglial activation was examined. Specific parameters measured to monitor microglial activation were nitric oxide (NO), prostaglandin E$_2$(PGE$_2$) and tumor necrosis factor-$\alpha$ (TNF-$\alpha$) release. Curcumin (1~10 $\mu$M) inhibited NO release induced by LPS and IFN-${\gamma}$ in a dose-dependent manner whereas 6-gingerol (2~20 $\mu$M) did not have any effect on LPS/IFN-${\gamma}$-induced NO release. The levels of PGE$_2$and TNF-$\alpha$ induced by LPS and IFN-${\gamma}$ were also inhibited by 1~10 $\mu$M curcumin in a dose-dependent manner. These results showed that curcumin could modulate microglial activation.

• 대한본초학회지
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• 제22권3호
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• pp.117-125
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• 2007

Objective : Lonicera japonica (Caprifoliaceae) has long been used for treatment of infectious diseases in oriental countries. The aim of this study was to investigative the effect by which the aqueous extract from flower of L. japonica (LJFAE) inhibited the lipopolysaccharide (LPS)-induced inflammatory mediators in murine macrophages, RAW 264.7 cells Methods : The dried flowers of L. japonica were extracted with distilled water at $100^{\circ}C$ for 7 h. The extract was filtered through 0.45 ${\mu}m$ filter, freeze-dried. The dried extract was dissolved in Hank's balanced salt solution (HBSS) and filtered through 0.22 ${\mu}m$ filter before use. Accumulated nitrite, an oxidative product of nitric oxide (NO), was measured in the culture medium by the Griess reaction. The levels of prostaglandin E2 (PGE2), tumor necrosis factor-$\alpha$ (TNF-$\alpha$), interleukin-1$\beta$ (IL-1$\beta$), and IL-6 production, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression were measured by enzyme-linked immunosorbent assay and Western blot analysis. Results: LJFAE (10-400 ${\mu}g$/ml) per se had no cytotoxic effect in unstimulated macrophages, but LJFAE concentration-dependently reduced NO, PGE2, TNF-, IL-l, and IL-6 production and COX-2 activity caused by stimulation of LPS. The levels of iNOS and COX-2 protein expressions were markedly suppressed by the treatment with LJFAE in a concentration dependent manner. Conclusions : These results suggest that LJFAE suppress the NO and PGE2production in macrophages by inhibiting iNOS and COX-2 expression and these properties may contribute to the anti-inflammatory activity of Lonicera japonica.

• Archives of Pharmacal Research
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• 제27권9호
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• pp.923-929
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• 2004

Stylopine is a major component of the leaf of Chelidonium majus L. (Papaveraceae), which has been used for the removal of warts, papillomas and condylomas, as well as the treatment of liver disease, in oriental countries. Stylopine per se had no cytotoxic effect in unstimulated RAW 264.7 cells, but concentration-dependently reduced nitric oxide (NO), prostaglandin E$_2$ (PGE$_2$), tumor necrosis factor-a (TNF-$\alpha$) and interleukin-1$\beta$(IL-1$\beta$), and the IL-6 production and cyclooxygenase-2 (COX-2) activity caused by the LPS stimulation. The levels of inducible nitric oxide synthase (iNOS) and COX-2 protein expressions were markedly suppressed by stylopine in a concentration dependent manner. These results suggest that stylopine suppress the NO and PGE$_2$ production in macrophages by inhibiting the iNOS and COX-2 expressions. These biological activities of stylopine may contribute to the anti-inflammatory activity of Cheli-donium majus.

• 대한의생명과학회지
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• 제18권3호
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• pp.237-243
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• 2012

This study was undertaken to know the effect of fat diet (for eight weeks) on changes of inflammatory markers [tumor necrosis factor (TNF-${\alpha}$) and prostaglandin $E_2$ ($PGE_2$)] and blood coagulation system [platelet aggregation function (PAF), prothrombin time (PT), activated partial thromboplastin time (aPTT)] in rats. Serum TNF-${\alpha}$, $PGE_2$, biochemical markers, PAF, PT, aPTT, and body weight were measured and compared between the control (normal diet-rats) and the fat group (fat diet-rats). The weights in the fat group were higher than those of the control group. TNF-${\alpha}$, $PGE_2$, glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatinine levels were greater in the fat group compared with the control group. The degree of platelet aggregation was lower, whereas PT and aPTT levels were longer in the fat group than in the control group. These findings have shown that fat diet may cause inflammatory response, diabetes, liver and renal dysfunction, and disturbances of fibrinolysis and coagulation system.