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Anti-inflammatory function of arctiin by inhibiting COX-2 expression via NF-κB pathways

BACKGROUND: Arctiin, isolated from Forsythia suspensa has been reported to have anti-inflammatory, anti-oxidant, antibacterial, and antiviral effects in vitro. However, there has been a lack of studies regarding its effects on immunological activity. The aim of this study is to investigate the anti-...

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Detalles Bibliográficos
Autores principales: Lee, Sungwon, Shin, Seulmee, Kim, Hyunyul, Han, Shinha, Kim, Kwanghee, Kwon, Jeunghak, Kwak, Jin-Hwan, Lee, Chong-Kil, Ha, Nam-Joo, Yim, Dongsool, Kim, Kyungjae
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146809/
https://www.ncbi.nlm.nih.gov/pubmed/21733191
http://dx.doi.org/10.1186/1476-9255-8-16
Descripción
Sumario:BACKGROUND: Arctiin, isolated from Forsythia suspensa has been reported to have anti-inflammatory, anti-oxidant, antibacterial, and antiviral effects in vitro. However, there has been a lack of studies regarding its effects on immunological activity. The aim of this study is to investigate the anti-inflammatory potential and possible mechanisms of arctiin in LPS-induced macrophages. METHODS: We investigated the mRNA and protein levels of proinflammatory cytokines through RT-PCR and western blot analysis, followed by a FACS analysis for surface molecule changes. RESULTS: Arctiin dose dependently decreased the production of NO and proinflammatory cytokines such as IL-1β, IL-6, TNF-α, and PGE(2), and it reduced the gene and protein levels as determined by RT-PCR and western blot analysis, respectively. The expression of co-stimulatory molecules such as B7-1 and B7-2 were also inhibited by arctiin. Furthermore, the activation of the nuclear transcription factor, NF-κB in macrophages was inhibited by arctiin. CONCLUSION: Taken together these results provide evidence of the bioactivity of arctiin in inflammatory diseases and suggest that arctiin may exert anti-inflammatory effect by inhibiting the pro-inflammatory mediators through the inactivation of NF-kB.