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Inflammation Research

Erschienen in:

01.07.2014 | Original Research Paper

Forsythin inhibits lipopolysaccharide-induced inflammation by suppressing JAK-STAT and p38 MAPK signalings and ROS production

verfasst von: Xiaolong Pan, Xiang Cao, Na Li, Yimiao Xu, Qiuyue Wu, Jing Bai, Zhimin Yin, Lan Luo, Lei Lan

Erschienen in: Inflammation Research | Ausgabe 7/2014

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Abstract

Objective

Forsythin (FOR) is an active ingredient extracted from the fruit of the medicinal plant Forsythia suspensa (Thunb.) Vahl. Here, we investigated the effect of FOR on LPS-induced inflammatory response and the underlying molecular mechanisms in RAW264.7 macrophages.

Materials and methods

RAW264.7 cells were pre-treated with or without FOR and then stimulated with or without LPS. The productions of TNF-α, IL-1β, IL-6, PGE₂ and NO were determined by ELISA and nitrite analysis, respectively. The expressions of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were measured by Western blotting and RT-PCR analysis. The activations of signaling molecules were detected by Western blotting using phosphorylation specific antibodies. Reactive oxygen species (ROS) production was determined by ROS assay.

Results

LPS-induced productions of IL-1β, IL-6, TNF-α, NO and PGE₂ were inhibited by FOR in a dose-dependent manner. FOR also suppressed the LPS-elevated expressions of iNOS and COX-2. Further investigations revealed that FOR significantly inhibited the LPS-induced activations of JAK-STATs and p38 MAPKs, but not of IKKα/β in LPS-stimulated RAW264.7 cells. Additionally, FOR interfered with both JAK-STATs and p38 MAPKs signaling pathways to modulate the expressions of IL-1β, IL-6, TNF-α, iNOS and COX-2. Furthermore, FOR reduced the LPS-induced ROS accumulation, validating that FOR serves as an antioxidant.

Conclusions

Our data suggested that FOR exerts anti-inflammatory action, at least in part, via suppressing LPS-induced activation of JAK-STATs and p38 MAPKs signalings and production of ROS in macrophage cells.

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Titel: Forsythin inhibits lipopolysaccharide-induced inflammation by suppressing JAK-STAT and p38 MAPK signalings and ROS production
verfasst von: Xiaolong Pan
Xiang Cao
Na Li
Yimiao Xu
Qiuyue Wu
Jing Bai
Zhimin Yin
Lan Luo
Lei Lan
Publikationsdatum: 01.07.2014
Verlag: Springer Basel
Erschienen in: Inflammation Research / Ausgabe 7/2014
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI: https://doi.org/10.1007/s00011-014-0731-7

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Abstract

Objective

Materials and methods

Results

Conclusions

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