Inhibitory effect of galanolactone isolated from Zingiber officinale roscoe extract on adipogenesis in 3T3-L1 cells
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Zingiber officinale Roscoe commonly known as ginger, has been used in traditional medicine. Inhibtion effect of galanolactone isolated from Z. officinale Roscoe on adipogenesis in 3T3-L1 cells was evaluated. Effect of galanolactone on 3T3-L1 adipocyte differentiation was measured by Oil Red O staining, and cytotoxicity effect of galanolactone was analyzed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay. The expression of various genes involved in adipogenic action of galanolactone was determined by real-time PCR and Western blot. Peroxisome proliferator-activated receptor γ (PPARγ) luciferase transactivation assay was used to evaluate the PPARγ transcriptional activity of galanolactone in HEK 293T cells. Galanolactone inhibited lipid accumulation and expression of adipocyte fatty acid-binding protein (aP2) and resistin in a dose-dependent manner in 3T3-L1 cells. Treatment with 50 and 100 μM of galanolactone significantly decreased the troglitazone-induced PPARγ transcripitional activity in HEK 293T cells, and suppressed expressions of PPARγ and CCAAT-enhancer-binding protein α (C/EBPα) at mRNA and protein levels in 3T3-L1 cells. These findings suggest that galanolactone isolated from Z. officinale Roscoe exerts anti-obesity effect through downregulation of adipogenic transcription factors and adipogenic marker genes.
Keywordsadipogenesis adipogenic marker genes galanolactone peroxisome proliferator-activated receptor γ 3T3-L1 cells Zingiber officinale
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- Fuhrman B, Rosenblat M, Hayek T, Coleman R, and Aviram M (2000) Ginger extract consumption reduces plasma cholesterol, inhibits LDL oxidation and attenuates development of atherosclerosis in atherosclerotic, apolipoprotein E-deficient mice. J Nutr 130, 1124–1131.Google Scholar
- Gregoire FM, Smas CM, and Sul HS (1998) Understanding adipocyte differentiation. Physiol Rev 78, 789–809.Google Scholar
- Kubota N, Terauchi Y, Miki H, Tamemoto H, Yamauchi T, Komeda K, Satoh S, Nakano R, Ishii C, Sugiyama T, Eto K, Tsubamoto Y, Okuno A, Murakami K, Sekihara H, Hasegawa G, Naito M, Toyoshima Y, Tanaka S, Shiota K, Kitamura T, Fujita T, Ezaki O, Aizawa S, Nagai R, Tobe K, Kimura S, and Kadowaki T (1999) PPAR gamma mediates high-fat dietinduced adipocyte hypertrophy and insulin resistance. Mol cell 4, 597–609.CrossRefGoogle Scholar
- Lehmann JM, Moore LB, Smith-Oliver TA, Wilkison WO, Willson TM, and Kliewer SA (1995) An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor γ (PPARγ). J Biol Chem 270, 12953–12956.Google Scholar
- Morrison RF and Farmer SR (2000) Hormonal Signaling and Transcriptional Control of Adipocyte Differentiation. J Nutr 130, 3116–3121.Google Scholar
- Rajala MW, Obici S, Scherer PE, and Rossetti L (2003) Adipose-derived resistin and gut-derived resistin-like molecule-beta selectively impair insulin action on glucose production. J Clin Invest 111, 225–230.Google Scholar
- Rosen ED, Walkey CJ, Puigserver P, and Spiegelman BM (2000) Transcriptional regulation of adipogenesis. Genes & Dev 14, 1293–1307.Google Scholar
- Tontonoz P, Hu E, Devine J, Beale EG, and Spiegelman BM (1995) PPARγ2 regulates adipose expression of the phosphoenolpyruvate carboxykinase gene. Mol Cell Biol 15, 351–357.Google Scholar