• The Journal of Internal Korean Medicine
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• v.28 no.1
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• pp.166-175
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• 2007

Objectives : This study was designed to evaluate the neuroprotective effect of Cirsium japonicum and Silibinin on lipopolysaccharide-induced inflammation in BV2 microglial cells. Methods : We studied on the neuroprotective effect of lipopolysaccharide-induced inflammation using MTS assay, western blot, and nitric oxide detection on mouse BV2 microglial cells. Results : Cirsium japonicum dose-dependently (50${\mu}g/ml$${\sim}$$250{\mu}g/ml$) inhibited nitrite production and iNOS expression in lipopolysaccharide-induced BV2 microglia and also significantly reduced lipopolysaccharide-induced COX-2 activation in western blot. Silibinin dose-dependently (10${\mu}M$${\sim}$$100{\mu}M$) inhibited nitrite production and iNOS expression in lipopolysaccharide-induced BV2 microglial cells. Silibinin also significantly reduced lipopolysaccharide-induced COX-2 activation in western blot. Conclusion : These effects of neuroprotection related to anti-inflammation suggest that Cirsium japonicum and Silibininmay be useful candidates for the development of a drug for related neurodegenerative diseases.

• Journal of Ginseng Research
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• v.37 no.1
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• pp.54-63
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• 2013

Ginsenoside Rd is a primary constituent of the ginseng rhizome and has been shown to participate in the regulation of diabetes and in tumor formation. Reports also show that ginsenoside Rd exerts anti-oxidative effects by activating anti-oxidant enzymes. Treatment with ginsenoside Rd decreased nitric oxide and prostaglandin $E_2$ ($PGE_2$) in lipopolysaccharides (LPS)-challenged RAW264.7 cells and in ICR mouse livers (5 mg/kg LPS; LPS + ginsenoside Rd [2, 10, and 50 mg/kg]). Furthermore, these decreases were associated with the down-regulations of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 and of nuclear factor (NF)-${\kappa}B$ activity in vitro and in vivo. Our results indicate that ginsenoside Rd treatment decreases; 1) nitric oxide production (40% inhibition); 2) $PGE_2$ synthesis (69% to 93% inhibition); 3) NF-${\kappa}B$ activity; and 4) the NF-${\kappa}B$-regulated expressions of iNOS and COX-2. Taken together, our results suggest that the anti-inflammatory effects of ginsenoside Rd are due to the down-regulation of NF-${\kappa}B$ and the consequent expressional suppressions of iNOS and COX-2.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.4
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• pp.1027-1031
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• 2006

In oriental medicine, Geijibokryunghwan(GBH) was used to improvement various symptoms created by the thrombosis. We investigated the effects of an oriental medicinal prescriptions, Geijibokryunghwan (GBH) consisting of herbs of Cinnamomi Ramufus (Geiji; 桂枝), Poria cocos (Bokrung; 茯?), Moutan Cortex Radicis(Modanpi; 牧丹皮), Paeoniae Radix (Jakyak; 芍藥) and Persicae Semen (Doin; 桃仁) on tumor growth-inhibitory activity and cancer chempreventive activity in assays representing three maior stages of carcinogenesis. Cancer chempreventive agents include nonsteroidal anti-inflammatory drugs (NSAIDS) such as indomethacin, aspirin, piroxicam, and sulindac, all of which inhibit cyclooxygenase (COX). Effects of the GBH extracts on carrageenan-induced edema Inflammation using female (C57BL/6XC3H) Fl (B6C3Fl ) mice and tumorigenesis were examined. Finally, cyclooxygenase metabolites were determined after extracts treatment. These data suggest that GBH extracts merits investigation as a potential cancer chempreventive agent in humans.

• Journal of Acupuncture Research
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• v.19 no.3
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• pp.41-50
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• 2002

Objective : To study anti-inflammatory, analgesic effect and molecular biological mechanism of honey bee venom for aqua-acupuncture, human mast cell line(HMC-1) and human glioma cell line(HS683) were treated with bee venom. Methods : Cell viability of bee venom was tested by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) asssay. To explore whether anti-inflammatory, analgesic effects of bee venom are associated with the control of gene expression, quantitative RT-PCR analysis of inflammation and pain related genes was performed. Results : The MTT assay demonstrated that cell viability was not decreased by treatment with 10-9 ug/ml bee venom in comparison with 10-2, 10-3, 10-4, 10-5, 10-6, 10-7, 10-8, 10-9, 10-10 and 10-11 ug/ml. sPLA2 and COX-l were down-regulated by treatment with 10-9 ug/ml bee venom in HS683 Cell line in comparison with control. COX-2 was up-regulated by treatment with 10-9 ug/ml bee venom in HS683 Cell line and HSP-2 was up-regulated by treatment with 10-9 ug/ml bee venom in HMC-1 Cell line in comparison with control. sPLA2, COX-1 and COX-2 showed no significant regulation in HMC-1 Cell line and cPLA2 also showed no significant regulation in both HMC-l and HS683 Cell line between control and bee venom treated group.

• Preventive Nutrition and Food Science
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• v.16 no.4
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• pp.299-306
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• 2011

The present study was designed to evaluate the inhibitory effects of fermented Liriope platyphylla extract on the production of inflammation-related mediators (NO, ROS, NF-${\kappa}B$, iNOS and COX-2) and pro-inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$, IL-6) in lipopolysaccharide-stimulated RAW 264.7 macrophages. Freeze-dried Liriope platyphylla was fermented by Saccharomyces cerevisiae and extracted with 70% ethanol. In lipopolysaccharide-stimulated macrophage cells, the treatment with fermented Liriope platyphylla extract decreased the generation of intracellular reactive oxygen species dose-dependently and increased antioxidant enzyme activities, including superoxide dismutase, catalase and glutathione peroxidase. Fermented Liriope platyphylla extract also inhibited NO production in lipopolysaccharide-stimulated RAW 264.7 cell. The expressions of NF-${\kappa}B$, iNOS, COX-2 and pro-inflammatory cytokines were inhibited by the treatment with fermented Liriope platyphylla extract. Thus, this study shows the fermented Liriope platyphylla extract could be effective at inhibiting the inflammation process.

• Archives of Pharmacal Research
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• v.26 no.12
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• pp.1061-1066
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• 2003

The fruit of Actinidia polygama (AP) has long been used as a folk medicine in Korea for treating pain, rheumatic arthritis and inflammation. The present investigation was carried out to determine the in vivo and in vitro anti-inflammatory activity of AP using several animal models of inflammation. The 70% ethanol extract of the fruit of AP significantly inhibited acetic acidinduced, vascular permeability in a dose dependent manner (23%, 38%, and 41 % inhibition at doses of 200 mg/kg, 500 mg/kg and 1000 mg/kg, respectively). This effect was maintained in AP water-soluble fraction (APW). The APW fraction also showed significant inhibitory activity against the rat paw edema induced by a single treatment of carrageenan. In vitro experiments were performed to demonstrate the inhibitory activities of APW (100 $\mu$ g/ml) on lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) production. The results showed that APW dose-dependently suppressed LPS-induced NO production in RAW 264.7 macrophages without a notable cytotoxic effect and also decreased inducible NO synthase (iNOS) protein expression. APW also showed a significant inhibitory effect in LPS-induced $PGE_2$ production and cyclooxygenase-2 (COX-2) expression.

• Nutrition Research and Practice
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• v.11 no.2
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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.

• Journal of Nutrition and Health
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• v.49 no.5
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• pp.288-294
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• 2016

Purpose: The aim of this work was to investigate the beneficial effects of rhamnazin against inflammation, reactive oxygen species (ROS)/reactive nitrogen species (RNS), and anti-oxidative activity in murine macrophage RAW264.7 cells. Methods: To examine the beneficial properties of rhamnazin on inflammation, ROS/ RNS, and anti-oxidative activity in the murine macrophage RAW264.7 cell model, several key markers, including COX and 5-LO activities, $NO^{\cdot}$, $ONOO^-$, total reactive species formation, lipid peroxidation, $^{\cdot}O_2$ levels, and catalase activity were estimated. Results: Results show that rhamnazin was protective against LPS-induced cytotoxicity in macrophage cells. The underlying action of rhamnazin might be through modulation of ROS/RNS and anti-oxidative activity through regulation of total reactive species production, lipid peroxidation, catalase activity, and $^{\cdot}O_2$, $NO^{\cdot}$, and $ONOO^{\cdot}$ levels. In addition, rhamnazin down-regulated the activities of pro-inflammatory COX and 5-LO. Conclusion: The plausible action by which rhamnazin renders its protective effects in macrophage cells is likely due to its capability to regulate LPS-induced inflammation, ROS/ RNS, and anti-oxidative activity.

• Journal of Ginseng Research
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• v.41 no.3
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• pp.240-246
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• 2017

Background: Korean Red Ginseng (KRG) is a traditional herbal medicine made by steaming and drying fresh ginseng. It strengthens the endocrine and immune systems to ameliorate various inflammatory responses. The cyclooxygenase-2 (COX-2)/prostaglandin E2 pathway has important implications for inflammation responses and tumorigenesis. Peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) is a transcription factor that regulates not only adipogenesis and lipid homeostasis, but also angiogenesis and inflammatory responses. Methods: The effects of the KRG on inhibition of hypoxia-induced COX-2 via $PPAR{\gamma}$ in A549 cells were determined by luciferase assay, Western blot, and/or quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The antimigration and invasive effects of KRG were evaluated on A549 cells using migration and matrigel invasion assays. Results and conclusion: We previously reported that hypoxia-induced COX-2 protein and mRNA levels were suppressed by KRG. This study examines the possibility of $PPAR{\gamma}$ as a cellular target of KRG for the suppression of hypoxia-induced COX-2. $PPAR{\gamma}$ protein levels and $PPAR{\gamma}$-responsive element (PPRE)-driven reporter activities were increased by KRG. Reduction of hypoxia-induced COX-2 by KRG was abolished by the $PPAR{\gamma}$ inhibitor GW9662. In addition, the inhibition of $PPAR{\gamma}$ abolished the effect of KRG on hypoxia-induced cell migration and invasion. Discussion: Our results show that KRG inhibition of hypoxia-induced COX-2 expression and cell invasion is dependent on $PPAR{\gamma}$ activation, supporting the therapeutic potential for suppression of inflammation under hypoxia. Further studies are required to demonstrate whether KRG activates directly $PPAR{\gamma}$ and to identify the constituents responsible for this activity.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.1-8
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• 2001

Increased expression of inducible cyclo-oxygenase (COX-2) is associated with a wide variety of tumours. In addition inhibitors of COX have shown a great deal of promise in vitro and in animal models as potential anti-tumour therapies. COX enzymes utilise the substrate arachidonic acid to produce prostaglandin (PO)H$_2$, the precursor to all the prostanoids.(omitted)