Nobiletin suppresses monocyte chemoattractant protein-1 (MCP-1) expression by regulating MAPK signaling in 3T3-L1 cells. (December 2016)

• Record Type: Journal Article
• Authors: Yasunaga, Sho; Domen, Miku; Nishi, Kosuke; Kadota, Ayumu; Sugahara, Takuya
• Is Part Of: Journal of functional foods. Volume 27(2016)
• Page Start: 406
• Page End: 415
• Publication Date: 2016-12
• Subjects: Nobiletin -- MCP-1 -- Chemokines -- Adipocyte hypertrophy -- 3T3-L1 cells -- Tumor necrosis factor α; Nobiletin (PubChem CID: 72344) -- 3-Isobutyl-1-methylxanthine (PubChem CID: 3758) -- Dexamethasone (PubChem CID: 5743); Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2016.09.025
• Languages: English
• ISSNs: 1756-4646

Abstract

Highlights: Nobiletin suppresses both gene expression and secretion of MCP-1 in 3T3-L1 adipocytes. Nobiletin downregulates ERK phosphorylation independent of differentiation stages. Nobiletin reduces MCP-1 secretion and ERK phosphorylation in TNF-α-treated adipocytes. Nobiletin may contribute to improving chronic inflammation in obese adipose tissues. Abstract: Nobiletin is a major citrus flavonoid possessing several biological activities. Nobiletin has been reported to display anti-inflammatory activity and to reduce monocyte chemoattractant protein (MCP)-1 secretion by 3T3-L1 adipocytes. However, its mode of action remains unclear. In the present study, we investigated the suppressive effect of nobiletin on MCP-1 expression in 3T3-L1 cells and its underlying molecular mechanism. Nobiletin notably down-regulated the MCP-1 mRNA level during adipocyte differentiation. Nobiletin also reduced MCP-1 secretion by preadipocytes (undifferentiated cells), differentiated adipocytes, and hypertrophied adipocytes. Immunoblot analysis showed that nobiletin inhibits the phosphorylation level of extracellular signal-regulated kinase (ERK) in both preadipocytes and differentiated adipocytes. Moreover, nobiletin suppressed MCP-1 secretion by adipocytes induced by tumor necrosis factor (TNF)-α.