β-glucan은 다양한 bacteria·균류·효모·버섯에서 생산되는 다당류로, 생산균주와 가지의 유/무, 결합위치 등에 따라 다양한 특성을 갖는 다당류가 된다. 흑효모인 Aureobasidium pullulans는 β-glucan을 세포외적으로 생산한다. A. pullulans에 의해 생산되는 β-(1,3)(1,6)-glucan은 항암, 항 알러지, 면역조절 활성 작용을 한다고 알려져 있다. 특히, 선천·후천면역 조절을 강화한다고 알려져 있으며, 이러한 효능으로 많은 국가에서 건강식품으로 소비되고 있다. 이에 따라, 본 연구는 ...
β-glucan은 다양한 bacteria·균류·효모·버섯에서 생산되는 다당류로, 생산균주와 가지의 유/무, 결합위치 등에 따라 다양한 특성을 갖는 다당류가 된다. 흑효모인 Aureobasidium pullulans는 β-glucan을 세포외적으로 생산한다. A. pullulans에 의해 생산되는 β-(1,3)(1,6)-glucan은 항암, 항 알러지, 면역조절 활성 작용을 한다고 알려져 있다. 특히, 선천·후천면역 조절을 강화한다고 알려져 있으며, 이러한 효능으로 많은 국가에서 건강식품으로 소비되고 있다. 이에 따라, 본 연구는 Escherichia coli LPS (E. coli LPS) 처리한 Macrophages인 RAW264.7 cells에서 염증성 매개 생산물에 대한 β-glucan 효과를 분석하였다. 배양 상층액을 이용하여 Nitric Oxide (NO) analysis 진행하였으며, inducible NO synthase (iNOS), heme oxygenase-1 (HO-1)mRNA 발현은 real-time polymerase chain reaction (PCR)을 이용하여 분석하였다. iNOS, HO-1, signal transducers and activators of transcription protein 1 (STAT1), Mitogen-activated protein kinases (MAPKs) protein인 c-Jun N-terminal Kinase (JNK), p38, Extracellular signal–regulated kinases (ERK) 단백질 발현와 Inhibitor κB-α (IκB-α) 분해를 Western blot analysis을 이용하여 평가하였으며, nuclear factor-κB (NF-κB)의 DNA 결합 활성은 ELISA-based assay kit와 western blot을 이용하여 분석하였다. E. coli LPS 유도로 활성화된 RAW264.7 cells에서 β-glucan은 iNOS로 유도된 NO을 억제하였으며, HO-1 발현을 증가시켰다. 그러나, β-glucan은 MAPKs protein인 JNK, p38, ERK 인산화에 영향을 미치지 않았으며, 또한, IκB-α 분해에 영향을 미치지 않았다. 대신에, β-glucan은 E. coli LPS에 유도된 STAT1 인산화가 급격히 억제되었다. 종합적으로, β-glucan은 E. coli LPS에 활성된 RAW264.7 cells에서 STAT1 pathway 억제와 HO-1 유도를 통해 NO 생산을 억제하였다. β-glucan은 숙주의 면역 반응 조절로 염증성 질환을 약화시키며, 효과적인 면역조절제로 이용할 수 있을 것이라 사려된다.
β-glucan은 다양한 bacteria·균류·효모·버섯에서 생산되는 다당류로, 생산균주와 가지의 유/무, 결합위치 등에 따라 다양한 특성을 갖는 다당류가 된다. 흑효모인 Aureobasidium pullulans는 β-glucan을 세포외적으로 생산한다. A. pullulans에 의해 생산되는 β-(1,3)(1,6)-glucan은 항암, 항 알러지, 면역조절 활성 작용을 한다고 알려져 있다. 특히, 선천·후천면역 조절을 강화한다고 알려져 있으며, 이러한 효능으로 많은 국가에서 건강식품으로 소비되고 있다. 이에 따라, 본 연구는 Escherichia coli LPS (E. coli LPS) 처리한 Macrophages인 RAW264.7 cells에서 염증성 매개 생산물에 대한 β-glucan 효과를 분석하였다. 배양 상층액을 이용하여 Nitric Oxide (NO) analysis 진행하였으며, inducible NO synthase (iNOS), heme oxygenase-1 (HO-1) mRNA 발현은 real-time polymerase chain reaction (PCR)을 이용하여 분석하였다. iNOS, HO-1, signal transducers and activators of transcription protein 1 (STAT1), Mitogen-activated protein kinases (MAPKs) protein인 c-Jun N-terminal Kinase (JNK), p38, Extracellular signal–regulated kinases (ERK) 단백질 발현와 Inhibitor κB-α (IκB-α) 분해를 Western blot analysis을 이용하여 평가하였으며, nuclear factor-κB (NF-κB)의 DNA 결합 활성은 ELISA-based assay kit와 western blot을 이용하여 분석하였다. E. coli LPS 유도로 활성화된 RAW264.7 cells에서 β-glucan은 iNOS로 유도된 NO을 억제하였으며, HO-1 발현을 증가시켰다. 그러나, β-glucan은 MAPKs protein인 JNK, p38, ERK 인산화에 영향을 미치지 않았으며, 또한, IκB-α 분해에 영향을 미치지 않았다. 대신에, β-glucan은 E. coli LPS에 유도된 STAT1 인산화가 급격히 억제되었다. 종합적으로, β-glucan은 E. coli LPS에 활성된 RAW264.7 cells에서 STAT1 pathway 억제와 HO-1 유도를 통해 NO 생산을 억제하였다. β-glucan은 숙주의 면역 반응 조절로 염증성 질환을 약화시키며, 효과적인 면역조절제로 이용할 수 있을 것이라 사려된다.
β-Glucan is a polysaccharide produced by bacteria, fungi, yeast and mushrooms. β-glucan in know to have antitumor and antiallergic activities. β-glucan in also know potent immuno-modulator an both innate and adaptive immunity. The effects of β-glucan were analyzed in RAW264.7 cells, murine macrophag...
β-Glucan is a polysaccharide produced by bacteria, fungi, yeast and mushrooms. β-glucan in know to have antitumor and antiallergic activities. β-glucan in also know potent immuno-modulator an both innate and adaptive immunity. The effects of β-glucan were analyzed in RAW264.7 cells, murine macrophage cell line, often lipopolysaccharide (LPS) treatment in this research. This present study used quantitative real-time polymerase chain reaction (RT-PCR) to quantify inducible NO synthase (iNOS), heme oxygenase-1 (HO-1) mRNA expression and NO activate were measured using incubated. The phosphorylation of mitogen-activated protein kinases (MAPKs), HO-1, iNOS, signal transducers and activators of transcription protein 1 (STAT1) and degradation of Inhibitor κB-α (IκB-α) were measured by Western blotting. The DNA-binding of the small unit of Nuclear factor-κB (NF-κB) was quantified by the enzyme-linked immunosorbent assay (ELISA) and western blot. In the RAW264.7 cells activated by E. coli LPS stimulation, the β-glucan inhibited the iNOS-derived NO. β-glucan increased the expression of the HO-1 in the cell that was stimulated by E. coli LPS, and the HO-1 in the RAW cells treated E. coli LPS activation was suppressed by the SnPP. The phosphorylation of MAPKs induced by the E. coli LPS were not impacted by the β-glucan, and the inhibitor κB (IκB)-α degradation was not impacted either. Instead, β-glucan remarkably inhibited the phosphorylation of the STAT1 that was induced by the E. coli LPS. Synthetically, the β-glucan suppressed the production of NO in the macrophages that was activated by the E. coli LPS through the STAT1 pathways inhibition and the HO-1 induction in this study. As the host immune response regulation by β-glucan attenuate the progress of the chronic inflammation, β-glucan can be used as an effective immuno-modulator.
β-Glucan is a polysaccharide produced by bacteria, fungi, yeast and mushrooms. β-glucan in know to have antitumor and antiallergic activities. β-glucan in also know potent immuno-modulator an both innate and adaptive immunity. The effects of β-glucan were analyzed in RAW264.7 cells, murine macrophage cell line, often lipopolysaccharide (LPS) treatment in this research. This present study used quantitative real-time polymerase chain reaction (RT-PCR) to quantify inducible NO synthase (iNOS), heme oxygenase-1 (HO-1) mRNA expression and NO activate were measured using incubated. The phosphorylation of mitogen-activated protein kinases (MAPKs), HO-1, iNOS, signal transducers and activators of transcription protein 1 (STAT1) and degradation of Inhibitor κB-α (IκB-α) were measured by Western blotting. The DNA-binding of the small unit of Nuclear factor-κB (NF-κB) was quantified by the enzyme-linked immunosorbent assay (ELISA) and western blot. In the RAW264.7 cells activated by E. coli LPS stimulation, the β-glucan inhibited the iNOS-derived NO. β-glucan increased the expression of the HO-1 in the cell that was stimulated by E. coli LPS, and the HO-1 in the RAW cells treated E. coli LPS activation was suppressed by the SnPP. The phosphorylation of MAPKs induced by the E. coli LPS were not impacted by the β-glucan, and the inhibitor κB (IκB)-α degradation was not impacted either. Instead, β-glucan remarkably inhibited the phosphorylation of the STAT1 that was induced by the E. coli LPS. Synthetically, the β-glucan suppressed the production of NO in the macrophages that was activated by the E. coli LPS through the STAT1 pathways inhibition and the HO-1 induction in this study. As the host immune response regulation by β-glucan attenuate the progress of the chronic inflammation, β-glucan can be used as an effective immuno-modulator.
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