Aucubin, a naturally occurring iridoid glycoside inhibits TNF-¦Á-induced inflammatory responses through suppression of NF-¦ÊB activation in 3T3-L1 adipocytes

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• 作者：Kyoung Sik Park ; ^{parkks@cju.ac.kr}
• 关键词：Iridoid glycoside ; Herbal medicine ; Adipocyte ; Inflammatory response
• 刊名：Cytokine
• 出版年：2013
• 出版时间：June, 2013
• 年：2013
• 卷：62
• 期：3
• 页码：407-412
• 全文大小：767 K

文摘

Obesity is closely associated with a state of chronic, low-grade inflammation characterized by abnormal cytokine production and activation of inflammatory signaling pathways in adipose tissue. Tumor necrosis factor (TNF)-¦Á is chronically elevated in adipose tissues of obese rodents and humans. Increased levels of TNF-¦Á are implicated in the induction of atherogenic adipokines, such as plasminogen activator inhibitor (PAI)-1, adipose-tissue-derived monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-6. Aucubin, an iridoid glycoside existing in medicinal plants, has been reported to show an anti-inflammatory activity by suppression of TNF-¦Á production in murine macrophages. The present study is aimed to investigate the effects of aucubin on TNF-¦Á-induced atherogenic changes of the adipokines in differentiated 3T3-L1 cells. Aucubin significantly inhibited TNF-¦Á-induced secretion and mRNA synthesis of the atherogenic adipokines including PAI-1, MCP-1, and IL-6. Further investigation of the molecular mechanism revealed that pretreatment with aucubin suppressed extracellular signal-regulated kinase (ERK) activation, inhibitory kappa B¦Á (I¦ÊB¦Á) degradation, and subsequent nuclear factor kappa B (NF-¦ÊB) activation. These findings suggest that aucubin may improve obesity-induced atherosclerosis by attenuating TNF-¦Á-induced inflammatory responses.