• Title/Summary/Keyword: Lipopolysaccharide

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The Inhibitory Activity of Erigeron annuus-Derived Components on $Interferon-{\gamma}$ and Lipopolysaccharide-Induced Nitric Oxide Production in Mouse Pheritoneal Macrophage

  • Lee, Hee-Jung;Kim, You-Ah;Jeong, Na-Ho;Hong, Seung-Heon;Seo, Young-Wan
    • Journal of Applied Biological Chemistry
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    • v.50 no.3
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    • pp.160-163
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    • 2007
  • Two flavonoids (1 and 2) and one phenolic acid (3) obtained from Erigeron annuus have recently been shown to have potent antioxidant activities. Aim of this study was to investigate the inhibitory effects of these components on $interferon-{\gamma}$ and lipopolysaccharide-induced nitric oxide productions in the mouse pheritoneal macrophage. Compounds 2 and 3 showed marked inhibitory activities against inducible nitric oxide synthase (iNOS) on the lipopolysaccharide and $interferon-{\gamma}-stimulated$ mouse pheritoneal macrophages without cytotoxicity. Therefore, these results suggest that the compounds could be effective anti-inflammatory agents as nitric oxide inhibitors in vivo.

Effect of Ginkgo biloba extract on the survival rate in lipopolysaccharide-induced sepsis model mice (Lipopolysaccharide로 유도한 패혈증 모델에서 Ginkgo biloba extract 투여가 생존율에 미치는 영향)

  • Rhee, Ki-Jong;Kim, Hyeon-Cheol;Jung, Bae-Dong
    • Korean Journal of Veterinary Service
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    • v.35 no.3
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    • pp.191-195
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    • 2012
  • Accumulated evidence indicate that Ginkgo biloba extract (EGb 761) acts as an antioxidant and scavenger of free radicals as well as influencing apoptotis. Earlier studies have employed the inflammatory agent lipopolysaccharide (LPS) to induce severe sepsis. In the present study, we examined whether the intraperitoneal injection of EGb 761 increases the survival rate of mice in the LPS-induced severe sepsis model. The survival rate was significantly increased by 30% in mice administered with 100 mg/kg of EGb 761 but not in mice administered with 50 mg/kg EGb 761. In addition, pre-treatment with EGb 761 increased the survival rate (30%) but post-treatment with EGb 761 did not. These results suggest that EGb 761 may have clinical potential in preventing sepsis induced mortality.

Anti-lipopolysaccharide antibody mitigates ruminal lipopolysaccharide release without acute-phase inflammation or liver transcriptomic responses in Holstein bulls

  • Mizuguchi, Hitoshi;Kizaki, Keiichiro;Kimura, Atsushi;Kushibiki, Shiro;Ikuta, Kentaro;Kim, Yo-Han;Sato, Shigeru
    • Journal of Veterinary Science
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    • v.22 no.3
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    • pp.34.1-34.7
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    • 2021
  • Anti-lipopolysaccharide (LPS) antibody administration has the potential benefits of neutralizing and consequently controlling rumen-derived LPS during subacute ruminal acidosis. Four Holstein bulls were used in this crossover study with a 2-week wash-out period. Anti-LPS antibody (0 or 4 g) was administered once daily for 14 days. Significantly lower ruminal LPS and higher 1-h mean ruminal pH were identified in the 4 g group. However, blood metabolites, acute-phase proteins, cytokines, and hepatic transcriptomes were not different between the two groups. Therefore, anti-LPS antibody administration mitigated ruminal LPS release and pH depression without accompanying responses in acute-phase inflammation or hepatic transcriptomic expression.

Regulation of Inflammatory Cytokine Production by Bee Venom in Rat Chondrocytes

  • Kim, Eun-Jung;Kim, Gye-Yeop
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.25 no.1
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    • pp.132-137
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    • 2011
  • Bee venom acupuncture (BVA), as a kind of herbal acupuncture, involved injecting diluted bee venom into acupoints and is used for pain, osteoarthritis and rheumatoid arthritis patients. BVA is growing in popularity, especially in Korea, and is used primarily for pain relief in many kinds of diseases. However, the effect of bee venom anti-inflammatory related action in lipopolysaccharide (LPS) induced chondrocyte stress have not been reported yet. The aim of this study was to investigate the effect of bee venom of cell viability and inflammatory cytokine in rat articular chondrocyte cultures stimulated with lipopolysaccharide. Inflammation was induced in rat chondrocytes by treatment with $10{\mu}g/m{\ell}$ LPS. The change of cell viability were decreased in chondrocytes after treatment with lipopolysaccharide. The cell viability revealed that BV exerted no significant cytotoxicity in the rat chondrocyte. Bee venom inhibited decreased cell viability in the presence of lipopolysaccharide ($10{\mu}g/m{\ell}$) in a dose dependent manner(0.1, 0.5, 1.0 and $5.0{\mu}g/m{\ell}$) at bee venom(p<0.05). Tumor necrosis factor (TNF)-${\alpha}$ production in the presence of lipopolysaccharide($1{\mu}g/m{\ell}$) was also inhibited in a dose dependent manner (p<0.05 from bee venom $0.1{\mu}g/m{\ell}$). Interleukin (IL)-6 production in the presence of lipopolysaccharide ($10{\mu}g/m{\ell}$) was inhibited as well (p<0.05 at bee venom 0.1, 0.5, 1.0 and $5.0{\mu}g/m{\ell}$, respectively). Our results demonstrate that bee venom was a anti-inflammatory agent of chondrocytes. Bee venom may exert its anti inflammatory effects through inhibition of TNF-${\alpha}$ and IL-6 synthesis, and may then pain relief and reduce the articular destruction.

IMMUNOSTIMULATION BY THE EXTRACTS OF SALICORNIA HERVACEA

  • Jeon, Young-Jin
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2002.05a
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    • pp.99-99
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    • 2002
  • In the present study, the potent lipopolysaccharide (LPS)-mimetic stimulation of B cells and macrophages by hot water extract from Salicornia herbacea (S. europeae L.) is described. The extract activated spleen cells to proliferate in a dose-related manner as measured by [$^3$ H)-thymidine incorporation response.(omitted)

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Anti-inflammatory effect of various solvent extract from Atractylodes japonica on Lipopolysaccharide-induced Inflammation in BV2 cells. (창출 추출물의 BV2 cell 소염작용에 관한 실험적 연구)

  • Hur, Inn-Hee;Sim, Sung-Yong;Kim, Kyung-Jun
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.20 no.2 s.33
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    • pp.36-46
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    • 2007
  • Objective : In this study, the effect of Atractylodes japonica against LPS induced inflammation in mouse microglia BV2 cells was investigated. Method : Microglia BV2 Cells viability was determined using the MTT assay. We used water, ethanol extract from Atractylodes japonica and studied on the anti-inflammatory effect of lipopolysaccharide-induced inflammation using reverse transcription polymerase chain reaction (RT-PCR), western blot, and nitric oxide detection on mouse microglia BV2 cells. Result : The MTT assay revealed that it's extract has no significant cytotoxicity in the microglia BV2 cell. Various solvent extract from Atractylodes japonica inhibited nitrite production, iNOS protein and mRNA expression levels. And also it's extracts significantly reduced lipopolysaccharide-induced COX-2 activation in RT-PCR and western blot in lipopolysaccharide-induced microglia BV2 cells Conclusion : In this study, it's extracts was shown to suppress NO production by inhibiting iNOS expression and COX-2 activity. With this effects of anti-inflammation, we suggests that, it's extracts may be a useful candidate for the development of a drug on the related inflammatory diseases in brain.

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Peroxynitrite Scavenging Activity of Sabohwanin Lipopolysaccharide-Induced Oxidatively-Stressed Mice (Lipopolysaccharide로 산화 스트레스를 유도한 Mouse에서 사보환(四補丸)의 Peroxynitrite 억제 효과)

  • Kweon, Youl;Jeong, Ji-Cheon
    • The Journal of Internal Korean Medicine
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    • v.28 no.1
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    • pp.80-91
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    • 2007
  • Objectives : Peroxynitrite (ONOO-), superoxide anion radical (?O2-) and nitric oxide (NO) are cytotoxic because they can oxidize several cellular components such as proteins, lipids and DNA. They have been implicated in the aging process, and age-related diseases such as Alzheimer's disease, rheumatoid arthritis, cancer and atherosclerosis. The aim of this study was to investigate Sabohwan's activity for scavenging ONOO- and its precursors. NO and ?02-. Methods : For this study, the fluorescent probes, namely 2',7'-dichlorodihydrofluorescein diacetate (DCFDA), 4.5-diaminofluorescein (DAF-2) and dihydrorhodamine 123 (DHR 123) were used. Results : Sabohwanblocked tert-butylhydroperoxide (t-BHP)-induced cell death in a dose-dependent fashion. It scavenged t-BHP-induced ONOO-, NO and ?O2- in YPEN cells. Sabohwan inhibited the generation of ONOO-, NO and ?O2- in the lipopolysaccharide (LPS)-treated mouse kidney postmitochondria both in vitro and in vivo. The lipid peroxide level increased and glutathione level decreased in the LPS-treated mice, whereas the ones in the Sabohwanadministered group among the LPS-treated mice reversed toward their natural levels. Conclusions : These results suggest that Sabohwanis an effective ONOO-, ?O2- and NO scavenger, and thereby it might have a potential role as a therapy against the aging process and age-related diseases.

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Inhibition by Higenamine of Lipopolysaccharide-induced iNOS mRNA Expression and NO Production in Rat Aorta (Lipopolysaccharide로 활성화시킨 흰쥐 혈관의 iNOS 발현에 대한 Higenamine의 효과)

  • Kang Young-Jin;Lee Goun-Woo;Ku Eui-Bon;Lee Hoi-Young;Chang Ki-Churl
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.3
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    • pp.297-302
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    • 1997
  • Higenamine was widely used as traditional remedy for the treatment of rhumatoid arthritis. Nitric oxide(NO) may be a critical mediator in this inflammatory disease. Synovial tissue from humans with inflammatory arthritis expresses NOS2(iNOS) mRNA and protein, and generates NO in vitro. We therefore, investigated the effect of higenamine on the induction of nitric oxide synthase(NOS) promoted by lipopolysaccharide(LPS). Prophylactic application of higenamine selectively prevented LPS-primed initiation of L-arginine-induced relaxation and restored rhenylephrine(PE)-induced contraction in rat aorta. LPS-stimulated nitrite production in the incubation medium was reduced by higenamine. Furthermore, RT-PCR and Northern analysis indicated that higenamine reduced iNOS expression primed by LPS in rat aorta. These results suggest that higenamine prevents LPS-promoted induction of NOS in vascular smooth muscle.

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