Inhibition of Nitric Oxide and Tumor Necrosis Factor-Alpha by Moutan Cortex in Activated Mouse Peritoneal Macrophages

Moutan cortex (MC) is one of the most widely used Oriental herbal medicines for treating inflammatory diseases. In this study, the effect of MC on lipopolysaccharide (LPS) and recombinant interferon-gamma (rIFN-γ)-induced production of nitric oxide (NO) and tumor necrosis factor (TNF)-alpha were exa...

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Veröffentlicht in:Biological & Pharmaceutical Bulletin 2007, Vol.30(5), pp.912-916
Hauptverfasser: Chung, Hwan-Suck, Kang, Moonkyu, Cho, Chongwoon, Parvez, Shoukat, Park, Chong-heong, Kim, Dongwoo, Oh, Joonghwan, Kim, Hongyeoul, Shin, Minkyu, Hong, Moochang, Kim, Yangseok, Bae, Hyunsu
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container_issue 5
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container_title Biological & Pharmaceutical Bulletin
container_volume 30
creator Chung, Hwan-Suck
Kang, Moonkyu
Cho, Chongwoon
Parvez, Shoukat
Park, Chong-heong
Kim, Dongwoo
Oh, Joonghwan
Kim, Hongyeoul
Shin, Minkyu
Hong, Moochang
Kim, Yangseok
Bae, Hyunsu
description Moutan cortex (MC) is one of the most widely used Oriental herbal medicines for treating inflammatory diseases. In this study, the effect of MC on lipopolysaccharide (LPS) and recombinant interferon-gamma (rIFN-γ)-induced production of nitric oxide (NO) and tumor necrosis factor (TNF)-alpha were examined using mouse peritoneal macrophages. MC inhibited the LPS/rIFN-γ-induced expression of inducible nitric oxide synthase (iNOS) and TNF-alpha release. To clarify the mechanism involved, the effect of MC on the activation of nuclear factor (NF)-kappaB was examined. The LPS/rIFN-γ-induced activation of NF-kappaB was almost completely blocked by MC at 0.5 mg/ml. These findings demonstrate that the inhibition of the LPS/rIFN-γ-induced production of NO and TNF-alpha by MC is due to the inhibition of NF-kappaB activation.
doi_str_mv 10.1248/bpb.30.912
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In this study, the effect of MC on lipopolysaccharide (LPS) and recombinant interferon-gamma (rIFN-γ)-induced production of nitric oxide (NO) and tumor necrosis factor (TNF)-alpha were examined using mouse peritoneal macrophages. MC inhibited the LPS/rIFN-γ-induced expression of inducible nitric oxide synthase (iNOS) and TNF-alpha release. To clarify the mechanism involved, the effect of MC on the activation of nuclear factor (NF)-kappaB was examined. The LPS/rIFN-γ-induced activation of NF-kappaB was almost completely blocked by MC at 0.5 mg/ml. 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subjects Animals
Anti-Inflammatory Agents, Non-Steroidal - pharmacology
anti-inflammatory effect
Blotting, Western
Cell Nucleus - drug effects
Cell Nucleus - enzymology
Cell Nucleus - metabolism
Cell Survival - drug effects
Cells, Cultured
Chromatography, High Pressure Liquid
Drugs, Chinese Herbal - pharmacology
Interferon-gamma - pharmacology
Lipopolysaccharides - pharmacology
Macrophage Activation - drug effects
Macrophages, Peritoneal - drug effects
Macrophages, Peritoneal - enzymology
Macrophages, Peritoneal - metabolism
Mice
Moutan cortex (MC)
NF-kappa B - metabolism
nitric oxide
Nitric Oxide - antagonists & inhibitors
Nitric Oxide Synthase Type II - antagonists & inhibitors
Paeonia
peritoneal macrophage
Recombinant Proteins
Tumor Necrosis Factor-alpha - antagonists & inhibitors
tumor necrosis factor-α
title Inhibition of Nitric Oxide and Tumor Necrosis Factor-Alpha by Moutan Cortex in Activated Mouse Peritoneal Macrophages
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