Aucubin, a naturally occurring iridoid glycoside inhibits TNF-alpha-induced inflammatory responses through suppression of NF-kappa B activation in 3T3-L1 adipocytes

作者：Park Kyoung Sik^*

来源：Cytokine, 2013, 62(3): 407-412.

DOI：10.1016/j.cyto.2013.04.005

• Iridoid glycoside
• Herbal medicine
• Adipocyte
• Inflammatory response

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)-alpha is chronically elevated in adipose tissues of obese rodents and humans. Increased levels of TNF-alpha 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-alpha production in murine macrophages. The present study is aimed to investigate the effects of aucubin on TNF-ce-induced atherogenic changes of the adipokines in differentiated 3T3-L1 cells. Aucubin significantly inhibited TNF-alpha-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 alpha (I kappa B alpha) degradation, and subsequent nuclear factor kappa B (NF-kappa B) activation. These findings suggest that aucubin may improve obesity-induced atherosclerosis by attenuating TNF-alpha-induced inflammatory responses.

• 出版日期2013-6