title: γ-Tocotrienol attenuates TNF-α-induced changes in secretion and gene expression of MCP-1, IL-6 and adiponectin in 3T3-L1 adipocytes.
abstract: Tocotrienols, members of the vitamin E family, have been shown to possess anti-inflammatory properties and display activity against a variety of chronic diseases, such as cancer, cardiovascular and neurological diseases. However, whether tocotrienols contribute to the prevention of inflammatory responses in adipose tissue remains to be elucidated. In this study, we examined the effects of γ-tocotrienol, the most common tocotrienol isomer, on tumor necrosis factor-α (TNF-α)-induced inflammatory responses by measuring the expression of the adipokines, monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6) and adiponectin in 3T3-L1 adipocytes. Exposure to TNF-α (10 ng/ml) for 24 h increased MCP-1 and IL-6 secretion, and decreased adiponectin secretion and peroxisome proliferator-activated receptor-γ (PPARγ) mRNA expression. γ-tocotrienol effectively improved the TNF-α-induced adverse changes in MCP-1, IL-6 and adiponectin secretion, and in MCP-1, IL-6, adiponectin and PPARγ mRNA expression. Furthermore, TNF-α-mediated IκB-α phosphorylation and nuclear factor-κB (NF-κB) activation were significantly suppressed by the γ-tocotrienol treatment. Our results suggest that γ-tocotrienol may improve obesity-related functional abnormalities in adipocytes by attenuating NF-κB activation and the expression of inflammatory adipokines.
authors.affiliation: Ajinomoto Integrative Research for Advanced Dieting, Graduate                     School of Agriculture, Kyoto University, Kyoto, Japan.
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Matsunaga
authors.forename: Ayae
authors.initials: A
authors.lastname: Shoji
authors.forename: Ning
authors.initials: N
authors.lastname: Gu
authors.forename: Erina
authors.initials: E
authors.lastname: Joo
authors.forename: Shiho
authors.initials: S
authors.lastname: Li
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Adachi
authors.forename: Hanae
authors.initials: H
authors.lastname: Yamazaki
authors.forename: Koichiro
authors.initials: K
authors.lastname: Yasuda
authors.forename: Takashi
authors.initials: T
authors.lastname: Kondoh
authors.forename: Kinsuke
authors.initials: K
authors.lastname: Tsuda
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D052242:Adiponectin / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D002839:Chromans / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000187:drug effects*; D051550:I-kappa B Kinase / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D014810:Vitamin E / Q000031:analogs & derivatives* / Q000494:pharmacology; D014815:Vitamins / Q000494:pharmacology
chemical_list: D052242:Adiponectin; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D002839:Chromans; D015850:Interleukin-6; D016328:NF-kappa B; D047495:PPAR gamma; D014409:Tumor Necrosis Factor-alpha; D014815:Vitamins; D014810:Vitamin E; C013649:plastochromanol 8; D051550:I-kappa B Kinase