• 제목/요약/키워드: lipopolysaccaride

검색결과 51건 처리시간 0.032초

마우스 비장세포에서의 Polychlorinated Biphenyls(Aroclor 1234)의 면역 독성 (Immunotoxicity of Polychlorinated Biphenyls (Aroclor 1254) in Mouse Splenocytes)

  • 반상자;안광수;김주환;임종준;김수연;기미경;이명숙;조수열;김영훈
    • Toxicological Research
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    • 제19권4호
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    • pp.277-283
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    • 2003
  • Polychlorinated biphenyls (PCBs) has been widely used as plasticizer, insulator, lubricant, paint and ink. The persistence of PCBs in the environment and their bioaccumulation in living organism make a raise concerns regarding their toxic effects in immune system and subsequent effects on human health. However little has been known about effect of PCB, an endocrine disrupter, on splenocytes. In this study, for identifying the effect on the organs and immune cell of mice by the concentration and time of commercial PCB mixture (Aroclor 1254), each 3 mice were tested at the concentration of 3, 30, 300, 1,000 mg/kg respectively, and their organ's weight were measured in 4, 7, 14 days, respectively. Also according to concentration and time, PCB was evaluated for the effects on splenocyte viability and lipopolysaccaride (LPS) and concanavaline A (Con A)-induced splenocyte proliferation on mice spleen. In liver and lung, there were significantly defferent by concentration and time of PCB (p < 0.0001). In respect of concentration of PCB, no significant effects on mice's liver by Aroclor 1254 concentration below than 300 mg/kg were observed except at the concentration of 1,000 mg/kg doses (p < 0.0001). But there was not significant different change in mice spleen by concentration and time of PCB (p=0.2206) and the mode of weight change of spleen was different to of liver and of lung. Viabilities of splenocytes were decreased following treatment with high concentration of PCB. Also, LPS and Con A-induced cell proliferations were decreased by Aroclor 1254 at 1,000 mg/kg. These data suggest that Aroclor 1254 is the immunotoxic compound that may have an effect on mouse immune system.

Regulation of Choline Transport by Oxidative Stress at the Blood-Brain Barrier In Vitro Model

  • Kang, Young-Sook;Lee, Hyun-Ae;Lee, Na-Young
    • Biomolecules & Therapeutics
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    • 제16권1호
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    • pp.14-20
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    • 2008
  • In the present study, we examined how the transport of choline is regulated at the blood-brain barrier (BBB) under the central nervous system (CNS) cellular damages by oxidative stress using a conditionally immortalized rat brain capillary endothelial cells (TR-BBB), in vitro the BBB model. It was also tested whether the choline uptake is influenced by membrane potential, extracellular pH, protonophore (FCCP) and amiloride in TR-BBB cells. In result, $[^3H]choline$ uptake was inhibited by FCCP and dependent on extracellular pH. The treatment of TR-BBB cells with 20 ng/mL tumor necrosis $factor-{\alpha}$ $(TNF-{\alpha})$, 10 ng/mL lipopolysaccharide (LPS), 100 ${\mu}M$ diethyl maleate (DEM) and 100 ${\mu}M$ glutamate resulted in 3.0-fold, 2.6-fold, 1.8-fold and 2.0-fold increases of $[^3H]choline$ uptake at the respective peak time, respectively. In contrast, hydrogen peroxide and raffinose did not show any significant effects on choline uptake. In addition, choline efflux was significantly inhibited by $TNF-{\alpha}$, LPS and DEM producing cell damage states. In conclusion, the influx and efflux transport system for choline existed in TR-BBB cell line and this process was affected by several oxidative stress inducing agents.

Sesquiterpene Derivatives Isolated from Cyperus rotundus L. Inhibit Inflammatory Signaling Mediated by NF-${\kappa}B$

  • Khan, Salman;Choi, Ran-Joo;Lee, Dong-Ung;Kim, Yeong-Shik
    • Natural Product Sciences
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    • 제17권3호
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    • pp.250-255
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    • 2011
  • The immune system is finely balanced by the activities of pro-inflammatory and anti-inflammatory mediators or cytokines. Unregulated activities of these mediators can lead to the development of various inflammatory diseases. A variety of safe and effective anti-inflammatory agents are available with many more drugs under development. Of the natural compounds, the sesquiterpenes (nootkatone, ${\alpha}$-cyperone, valencene and ${\alpha}$-selinene) isolated from C. rotundus L. have received much attention because of their potential antiinflammatory effects. However, limited studies have been reported regarding the influence of sesquiterpene structure on anti-inflammatory activity. In the present study, the anti-inflammatory potential of four structurally divergent sesquiterpenes was evaluated in lipopolysaccaride (LPS)-stimulated RAW 264.7 cells, murine macrophages. Among the four sesquiterpenes, ${\alpha}$-cyperone and nootkatone, showed stronger anti-inflammatory and a potent NF-${\kappa}B$ inhibitory effect on LPS-stimulated RAW 264.7 cells. Molecular analysis revealed that various inflammatory enzymes (iNOS and COX-2) were reduced significantly and this correlated with downregulation of the NF-${\kappa}B$ signaling pathway. Additionally, electrophoretic mobility shift assays (EMSA) elucidated that nootkatone and ${\alpha}$-cyperone dramatically suppressed LPS-induced NF-${\kappa}B$-DNA binding activity using 32Plabeled NF-${\kappa}B$ probe. Hence, our data suggest that ${\alpha}$-cyperone and nootkatone are potential therapeutic agents for inflammatory diseases.

The Methanol Extract of Azadirachta indica A. Juss Leaf Protects Mice Against Lethal Endotoxemia and Sepsis

  • Kim, Woong-Hyun;Song, Hyun-Ok;Jin, Chun-Mei;Hur, Jong-Moon;Lee, Hwa-Sung;Jin, Han-Yong;Kim, Sung-Yeon;Park, Hyun
    • Biomolecules & Therapeutics
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    • 제20권1호
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    • pp.96-103
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    • 2012
  • In the present study, the inhibitory effect of neem leaf extract (NLE) on lipopolysaccaride (LPS)-induced nitric oxide (NO) and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) production was examined both in vitro and in vivo. In vitro study revealed that NLE treatment ($100{\mu}g/ml$) inhibits LPS (100 ng/ml)-induced NO production by 96% and TNF-${\alpha}$ production by 32%. The reduction in NO production is probably conferred by the complete suppression of inducible nitric oxide synthase (iNOS) expression. Interestingly, in vivo NLE significantly improved the survival rate of mice in an experimental sepsis model. Administration of NLE (100 mg/kg) 24 h before LPS treatment (20 mg/kg) improved the survival rate of mice by 60%. The inhibition of plasma NO and TNF-${\alpha}$ production by NLE is likely to account for the improved survival of mice. Our results suggest that NLE may present a promising avenue in the development of therapeutic agents for the treatment of inflammatory diseases.

사료중 어유가 급성기 반응중인 육계 병아리에서 에너지 대사와 항산화효소 활성에 미치는 영향

  • 박인경;김재환;임진택;이성일;고태송
    • 한국가금학회:학술대회논문집
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    • 한국가금학회 2003년도 제20차 정기총회 및 학술발표회
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    • pp.73-74
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    • 2003
  • 육계 병아리에서 어유 함유사료 급여에 의한 급성기 반응중의 생산성 감소 완화와 단백질 대사, 에너지 대사 및 항산화효소 활성의 관계를 조사하였다. 병아리에 1일령부터 어유 사료를 급여하면 급성기 반응중에 에너지 밸런스를 높이나 성장률, 요산 배설량과 질소 밸런스가 낮아지지 않았으며, 대두유 함유 사료를 급여한 것에 비하여 간장과 적혈구 세포액의 SOD 활성을 높였다. 이러한 결과는 어유 함유사료 급여로 급성기 반응중의 증체량 감소가 완화되는 효과는 항산화효소계의 조정과 에너지 급원의 소화관내 흡수 증가에 기인한다는 것을 나타낸다.

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다시마섭취가 정상과 당뇨 생쥐 대식세포의 Cytokine 분비에 미치는 영향 (Effect of Sea Tangel Intake on Cytokine Production in Macrophage from Normal and Diabetic Mice)

  • 조성희;양경미;배복선;임선아;유리나
    • 한국식품영양과학회지
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    • 제27권5호
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    • pp.952-959
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    • 1998
  • To investigate the effect of sea tangle on macrophage activity in normal and diabetic states, 10week old ICR mice were fed control(C) and sea tangle(S) diet containing 5%(w/w) cellulose and 13.6%(w/w) dry sea tangle for four weeks, after which two thirds of mice(CD and SD) were made diabetic by intramuscular injection of streptozotocin(150mg/kg bw). At 4th day after diabetes was apparent by urinary glucose, one half of diabetic mice(CDM and SDM) were treated with metformin(500mg/kg bw) orally. Peritoneal macrophages obtained from 3%-thioglycollate treated mice were cultured in the presence of lipopolysaccaride from Salmonella abortus equi(10$\mu\textrm{g}$/ml) for 24 hrs and tumor necrosis factor-$\alpha$(TNF$\alpha$), interleukin-1$\beta$(1L-1$\beta$)and prostaglandin E2(PGE2) were measured in culture media. Release of IL-1$\beta$and PGE2 from macrophage were increased in normal mice by sea tangle diet and had the same tedency in diabetic mice with or without metformin treatment although not statistically significant. Release of TNF$\alpha$ tended to be reduced by diabetes but were not changed significantly by sea tangle diet. Fatty acid compositions of macrophage and liver phospholipids showed that diabetes reduced arachidonic acid/linoleic acid ratio and sea tangle diet appeared to increase contentsof polyunsaturated fatty acids.

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Lipopolysaccharide 유도된 Raw264.7 세포주에서 전사조절인자 NF-κB와 IRF-1의 공동작용에 의해 조절되는 PD-1 발현연구 (PD-1 Expression in LPS-Induced Raw264.7 Cells Is Regulated via Co-activation of Transcription Factor NF-κB and IRF-1)

  • 최은경;이수운;이수웅
    • 미생물학회지
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    • 제49권4호
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    • pp.301-308
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    • 2013
  • Programmed Death-1 (PD-1)은 중요한 면역조절분자들 중 하나로 다양한 면역활성인자에 자극된 T 세포, B 세포, NKT 세포 및 대식세포에서 발현된다. Lipopolysaccaride (LPS)는 그람음성세균의 세포벽구성물질로 PD-1 발현을 유도하는 중요 면역원들 중 하나로 알려져 있다. 그러나 선천면역세포에서 PD-1 발현기전에 관한 연구는 미비한 실정이다. 본 연구에서는 LPS에 의해 자극된 Raw264.7 세포주를 대상으로 PD-1 발현 및 발현조전기전을 RT-PCR, Western Blot, 유세포분석기, ChIP assay 및 co-immunoprecipitation 방법으로 조사하였다. Raw264.7 세포주가 LPS로 자극되었을 때 PI3K 및 p38 신호전달경로를 경유하여 PD-1 발현이 크게 증가되었다. 또한 LPS 주사된 생쥐의 비장유래 대식세포에서도 PD-1 발현이 증가됨을 확인 하였다. PD-1 유전자의 프로모터 분석을 통해서 NF-${\kappa}B$ 및 IRF-1 결합부위가 PD-1 발현에 중요함을 알 수 있었다. 또한 PD-1 발현을 극대화하기 위하여 전사조절인자 NF-${\kappa}B$ 및 IRF-1의 공동활성이 필수적임을 확인하였다. 본 연구결과는 LPS 유도 생쥐패혈증모델에서 선천면역세포에 발현된 PD-1분자의 제어를 통한 질병 연구에 유용한 자료로 이용될 수 있을 것으로 사료된다.

The Effect of Dohongsamul-tang on Cytokine Production in Peripheral Blood Monocular Cells of Patients with Acute Cerebral Infarction

  • Park, Sae-Wook;Lee, Sun-Woo;Kang, Baek-Gyu;Lee, In;Cho, Kwang-Ho;Moon, Byung-Soon
    • 대한한의학회지
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    • 제27권4호
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    • pp.1-11
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    • 2006
  • Objectives : We investigated the effect of Dohongsamul-tang (DHSMT) on the production of various cytokines in lipopolysaccaride (LPS) stimulated peripheral mononuclear cells (PBMCs) from CI patients. Methods: Cell viability was determined using MTT assay. ELISA was carried out for investigating $TNF-{\alpha}$, $IL-1{\beta}$, IL-6, IL-8, IL-4, and $TGF-{\beta}$ 1 Results : The amount of tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$, IL-6, IL-8, IL-4, and transforming growth factor(TGF)-${\beta}$ 1 in PBMC culture supernatant significantly increased in the LPS treated cells compared to unstimulated cells. We show that DHSMT inhibited the production of TNF-${\alpha}$, IL-1${\beta}$, IL-6, IL-8, and IL-4 induced by LPS in a dose dependent manner. The maximal inhibition rate of the TNF-${\alpha}$, IL-1${\beta}$, IL-6, IL-8, and IL-4 production by pretreatment of DHSMT (1.0mg/ml) was 38.52 ${\pm}$ 2.5% (P < 0.01), 44.02 ${\pm}$ 3.5% (P < 0.05), 45.32 ${\pm}$ 2.3% (P < 0.01), 42.30 ${\pm}$ 3.1% (P < 0.05), and 49.70 ${\pm}$ 3.1%(P &lt; 0.05), respectively. On the other hand, DMSMT significantly increased the LPS-induced TGF-${\beta}$ 1 production(P<0.05). Conclusions : Taken together. these results suggest that DHSMT might have regulatory effects on cytokine production, which might explain its beneficial effect in the treatment of CI.

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별갑이 아토피 피부염에서의 알러지성 염증 반응에 미치는 영향 (Effects of Amyda sinensis on Allergic Inflammation Mechanism related Atopy Dermatitis)

  • 심태경;고대경;김현창;백연종;이재석;유화승
    • 혜화의학회지
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    • 제20권1호
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    • pp.69-83
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    • 2011
  • Objectives: This study aimed to investigate the effects of Amyda sinensis (AS) on allergic inflammation mechanism related atopy dermatitis. Methods: To investigate the effects of AS, We study inhibitory effect of AS on the levels of pro-inflammatory cytokines released from Raw264.7 cell stimulated with LPS (lipopolysaccaride), and EoL-1, THP-1, Jutkat cell stimulated with DP (Dermatophagoides pteronyssinus), and LPS indused acute inflammatory BALB/c mouse model. Result: AS reduced the levels of IL-$1{\beta}$ released from Raw264.7 cell stimulated with LPS at 20 ug/ml, 5 ug/ml concentration, and reduced the levels of IL-6 in a dose-dependent. AS significantly reduced the levels of MCP-1 released from EoL-1 cell stimulated with DP (Dermatophagoides pteronyssinus) at all the concentration, and significantly reduced the level of IL-8 at 0.1 ug/ml concentration. AS significantly reduced the levels of MCP-1 released from THP-1 cell stimulated with DP (Dermatophagoides pteronyssinus) at 1 ug/ml concentration, and reduced the level of IL-6 in a dose-dependent. AS significantly reduced the levels of IL-4 released from Jutkat cell stimulated with DP at all the concentration, and significantly reduced the level of IL-5 at 0.1 ug/ml. 1 ug/ml concentration,. and reduced the level of TNF-${\alpha}$ in a dose-dependent. AS significantly reduced the levels of TNF-${\alpha}$, IL-6, IL-$1{\beta}$, in LPS indused acute inflammatory BALB/c mouse model, in a dose-dependent. Conclusion: These result suggested that AS has suppressive effect on pro-inflammatory cytokines in various cell lines through the regulation of immune system. AS could be applied on the medicinal sources for treatment of immune abnormal diseases such as atopy dermatitis afterward.

Transduced PEP-1-AMPK inhibits the LPS-induced expression of COX-2 and iNOS in Raw264.7 cells

  • Shin, Min-Jea;Lee, Yeom-Pyo;Kim, Dae-Won;An, Jae-Jin;Jang, Sang-Ho;Cho, Sung-Min;Sheen, Seung-Hoon;Lee, Hae-Ran;Kweon, Hae-Yong;Kang, Seok-Woo;Lee, Kwang-Gill;Park, Jin-Seu;Eum, Won-Sik;Cho, Yong-Jun;Choi, Soo-Young
    • BMB Reports
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    • 제43권1호
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    • pp.40-45
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    • 2010
  • AMP-activated protein kinase (AMPK) is a heterotrimeric enzyme that plays a central role in cellular metabolic stress. Modulation of nitric oxide (NO) and cyclooxygenase-2 (COX-2) is considered a promising approach for the treatment of inflammation and neuronal diseases. In this study, the AMPK gene was fused in-frame with PEP-1 peptide in a bacterial expression vector to produce a PEP-1-AMPK fusion protein. Expressed and purified PEP-1-AMPK fusion proteins were transduced efficiently into macrophage Raw 264.7 cells in a time- and dose-dependent manner. Furthermore, transduced PEP-1-AMPK fusion protein markedly inhibited LPS-induced iNOS and COX-2 expression. These results suggest that the PEP-1-AMPK fusion protein can be used for the protein therapy of COX-2 and NO-related disorders such as inflammation and neuronal diseases.