• 제목/요약/키워드: IFN-ν

검색결과 5건 처리시간 0.018초

Inulin stimulates NO synthesis via activation of PKC-$\alpha$ and protein tyrosine kinase, resulting in the activation of NF-$textsc{k}$B by IFN-ν-primed RAW 264.7 cells

  • Koo, Hyun-Na;Hong, Seung-Heon;Kim, Hyung-Min
    • 한국응용약물학회:학술대회논문집
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    • 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
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    • pp.78-78
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    • 2003
  • Inulin, an active component of Chicorium intybus root, has been shown to stimulate the growth of bifidobacteria, and inhibit colon carcinogenesis. NO mediates a number of the host-defense functions of activated macrophages, including antimicrobial and tumoricidal activity. We examined the effect of inulin on the synthesis of NO in RAW 264.7 cells. Inulin alone had no effect, whereas inulin with IFN-ν synergistically increased the NO production and inducible NO synthase (iNOS) expression in RAW 264.7 cells. Synergy between IFN-ν and inulin was mainly dependent on inulin-induced TNF-${\alpha}$ secretion. Also, protein kinase C (PKC)-${\alpha}$ was involved in the inulin-induced NO production. Inulin-mediated NO production was inhibited by the protein tyrosine kinase (PTK) inhibitor, tyrphostin AG126. Since iNOS gene transcriptions have been shown to be under the control of the NF -$\kappa$B/Rel family of transcription factors, we assessed the effect of inulin on NF -$\kappa$B/Rel using an EMSA. Inulin produced strong induction of NF-$\kappa$B/Rel binding, whereas AP-l binding was slightly induced in RAW 264.7 cells. Inulin stimulated phosphorylation and degradation of I$\kappa$B-${\alpha}$. These results suggest that in IFN-ν-primed RAW 264.7 cells inulin might stimulate NO synthesis via activation of PKC-${\alpha}$ and PTK, resulting in the activation of NF-$\kappa$B.

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The effect of Astragali Radix Ethanol extract on Murine CD4 T cells′ Cytokine Profiles in vitro

  • Hee Kang;Bae Hyun Su;Ahn Kyoo Seok
    • 동의생리병리학회지
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    • 제17권5호
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    • pp.1330-1334
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    • 2003
  • Astragali Radix(AR), one of the strong tonic herbs, is known to improve immunological responses in mice and human. In this study, AR's ai-reinforcing effect was examined in the context of CD4/sup +/ T cells' TCR/CD3 induced activation responses. In order to evaluate the direct effect of AR on helper T cells, CD4/sup +/ T cells are isolated using magnetic bead and their proliferation and CD69 expression in AR treated medium were assessed with anti-CD3/anti-CD28 activation for 48h. CD4 T cells' proliferation was slightly increased but there was little effect on CD69 expression. RT PCR and ELISA equally demonstrated that IL-2 and IL-4 production was increased but IFN-ν was down-regulated. This shows AR ethanol extract favors Th2 cytokine profile under neutral conditions.

사료내 감태 및 감태로부터 추출한 crude lectin의 첨가가 육계의 생산성 및 면역반응에 미치는 영향

  • 김성권;유선종;안병기;박근규;이훈택;송창선;허억;강창원
    • 한국가금학회:학술대회논문집
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    • 한국가금학회 2004년도 제21차 정기총회 및 학술발표회
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    • pp.23-25
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    • 2004
  • 본 실험은 감태와 crude lectin의 사료내 첨가가육계의 생산성 및 면역반응에 미치는 영향을 조사하기 위하여 실시하였다. 1일령 Ross 수평아리 총234수를 공시하여 대조구(-), 대조구(+), 감태 1.0%, crude lectin 0.05 %, 0.1 %, 및 0.3 %로 6처리 3반복, 반복당 13수씩을 총 38일간 실험사료를 급여하였고, ND-IB 혼합 사독백신은 4일령에 피하접종하였다. 사료요구율에 있어서는 crude lectin 0.3 % 첨가구가 대조구(-)에 비해 유의하게 낮게 나타났다(P<0.05). ND-IB 사독 혼합백신 접종 3주 후에는 감태와 crude lectin의 첨가구의 ND와 IB 백신 역가가 대조구(+)와 비교하여 상승하는 경향이나 상승효과가 있었다(P<0.05). 폐사율에 있어서 crude lectin 첨가구들은 살모넬라를 감염시킨 대조구(+)에 비해 유의하게 감소하였다(P<0.05). 닭에서 IFN-v, IL-2, 및 IL-6의 mRNA는 살모넬라 감염에 의해 높게 발현되었고, 감태와 crude lectin은 IFN-v의 발현에 영향을 미치지 않았으나, 감태 1.0 %와 crude lectin 0.05 % 첨가구는 IL-2와 IL-6의 mRNA 농도가 대조구(+)에 비해 높은 경향이나 유의하게 높았다(p<0.05).

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Extracellular Signal-Regulated Kinase (ERK1/2) Regulate Glucose Deprivation-Induced Cell Death in Immunostimulated Astrocytes

  • Yoo, Byoung-Kwon;Park, Ji-Woong;Yoon, Seo-Young;Jeon, Mi-Jin;Park, Gyu-Hwan;Chun, Hyun-Joo;Ko, Kwang-Ho
    • 한국응용약물학회:학술대회논문집
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    • 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
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    • pp.83-83
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    • 2003
  • In our previous study, glucose deprivation was reported to induce the potentiated death and ATP loss in immunostimulated astroglia. And this vulnerability to glucose deprivation was due to overproduction of nitric oxide (NO) and hydrogen peroxide (H$_2$O$_2$). In the present study, the role of extracellular signal-regulated kinase 1/2 (ERK1/2) in the glucose deprivation-induced death of immunostimulated astroglia was examined. We showed that immunostimulation with LPS+IFN-ν activated the ERKl/2 signal pathway and produced a large amount of NO and H$_2$O$_2$. Generation of NO and H$_2$O$_2$ in immunostimulated astroglia was mediated via ERK1/2 signal pathways, since addition of the ERK kinase (MEKl) inhibitor PD98059 reduced NO and H$_2$O$_2$production. ERK1/2 activation-mediated NO and H$_2$O$_2$ production is due to an activation of iNOS and NADPH oxidase, respectively. Finally, we found that glucose deprivation caused ATP depletion and the augmented death in immunostimulated astroglia, which was also prevented by PD98059 treatment. These results demonstrate that the ERK1/2 signal pathways play an important role in glucose deprivation induced the death in immunostimulated astroglia by regulating the generation of NO and H$_2$O$_2$.

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