タデ藍Persicaria tinctoria 含有Tryptanthrin によるPPARγ活性化と3T3-L1 細胞の脂肪細胞分化の促進による細胞内脂肪滴蓄積の減少について

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  • Tryptanthrin Promotes Adipocyte Differentiation and Reduces Lipid Accumulation in 3T3-L1 Cells via Peroxisome Proliferator-Activated Receptor γ
  • タデ アイ Persicaria tinctoria ガンユウ Tryptanthrin ニ ヨル PPARgカッセイカ ト 3T3-L1 サイボウ ノ シボウ サイボウ ブンカ ノ ソクシン ニ ヨル サイボウ ナイ シボウ テキ チクセキ ノ ゲンショウ ニ ツイテ

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説明

The number of obesity and type 2 diabetes mellitus（T2DM）patients is increasing worldwide. T2DM ischaracterized by the decreasing of insulin sensitivity and insufficient insulin release from pancreatic β-cells caused by insulin resistance. in addition, impaired adipocyte differentiation enhances insulin resistance. as the peroxisome proliferator-activated receptorγ（PParγ）plays an important role in insulin sensitivity and adipocyte differentiation, the thiazolidine drugs which are known to PParγagonist can clinically improve insulin resistance. Persicaria tinctoria has been used as a dye and traditional Japanese medicine in Japan over the years. Tryptanthrin, which is an ingredient of this plant is reported to have a variety of bioactivity such as antibacterial, anti-cancer, and anti-inflammatory. recently, Persicaria tinctoria is also used as edible food, and its usefulness has attracted attention. Thus, to investigate the effect of tryptanthrin on the cell differentiation and adipogenesis process in 3T3-L1 cells, 3T3-L1 cells were cultured to determine the effect of cell differentiation and glucose uptake with tryptanthrin. as a result, tryptanthrin enhanced adipocyte differentiation in 3T3-L1 cells similar to rosiglitazone. This effect was inhibited by cotreatment with GW9662, a PParγ antagonist. in mature 3T3-L1 adipocytes, the lipid droplet size and accumulation were reduced by this compound and observed micro lipid droplets. The glucoseconsumption were also significantly increased. in conclusion, this finding suggested that tryptanthrin is a potential anti-diabetic compound for T2DM by promoting adipocyte differentiation and glucose consumption via PPAR γ.

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