title: 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.
authors.affiliation: Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.
authors.forename: Sun-Young
authors.initials: SY
authors.lastname: Nam
authors.affiliation: Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea. Electronic address: hmkim@khu.ac.kr.
authors.forename: Hyung-Min
authors.initials: HM
authors.lastname: Kim
authors.affiliation: Department of Food Technology and Biochip Research Center, Hoseo University, Asan, Chungnam, 336-795, Republic of Korea. Electronic address: hjjeong@hoseo.edu.
authors.forename: Hyun-Ja
authors.initials: HJ
authors.lastname: Jeong
mesh_terms: D020170:Caspase 1 / Q000235:genetics / Q000378:metabolism*; D002454:Cell Differentiation; D002470:Cell Survival; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D005960:Glucosides / Q000494:pharmacology*; D006801:Humans; D007378:Interleukins / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects* / Q000502:physiology; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II; D010636:Phenols / Q000494:pharmacology*; D059808:Polyphenols
chemical_list: D020170:Caspase 1; D016207:Cytokines; D005960:Glucosides; D007378:Interleukins; D008070:Lipopolysaccharides; D016328:NF-kappa B; D052247:Nitric Oxide Synthase Type II; D010636:Phenols; C496971:IL32 protein, human; C058956:acteoside; D059808:Polyphenols
keywords: Acteoside; IL-32; Inflammatory reactions; Macrophage differentiation; Thymic stromal lymphopoietin