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Attenuation of IL-32-induced caspase-1 and nuclear factor-κB activations by acteoside.

Abstract：

:Acteoside has anti-inflammatory and antioxidant potentials. Nevertheless, little information is available about the pharmacological mechanism of acteoside. Here, we report the regulatory effects and underlying mechanisms of acteoside on interleukin (IL)-32-induced inflammatory reactions using human monocytes cells line, THP-1 cells. Acteoside suppressed IL-32-induced macrophage-like cells differentiation. Levels of thymic stromal lymphopoietin, tumor necrosis factor (TNF)-α, IL-1β, and IL-8 increased by IL-32 or LPS were significantly reduced by treatment with acteoside in THP-1 cells. Acteoside attenuated IL-32-induced caspase-1 and nuclear factor-κB activations in THP-1 cells. In IL-32-induced macrophages, acteoside significantly reduced LPS-induced TNF-α, IL-1β, IL-6, and IL-8 production. In addition, production of nitric oxide (NO) and expression of inducible NO synthase increased by LPS were significantly decreased by treatment with acteoside in IL-32-induced macrophages. Our data suggest that acteoside exhibits an anti-inflammatory activity by suppressing IL-32 signaling pathway. Collectively, the results indicate that acteoside may act as a regulator of the IL-32 induced immune responses.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Nam SY,Kim HM,Jeong HJ

doi

10.1016/j.intimp.2015.09.026

subject

Has Abstract

pub_date

2015-12-01 00:00:00

pages

574-582

issue

2

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(15)30129-6

journal_volume

29

pub_type

杂志文章

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