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. Author manuscript; available in PMC: 2017 Jul 29.
Published in final edited form as: Exp Biol Med (Maywood). 2011 Nov 23;236(12):1379–1388. doi: 10.1258/ebm.2011.011234

Figure 5.

Figure 5

Homocysteine (Hcy) suppressed rosiglitazone-induced adipogenesis in 3T3-L1 preadipocytes. Two days after plating (D0), 3T3-L1 preadipocytes were exposed to differentiation medium containing isobutylmethylxanthine, dexamethasone and rosiglitazone (MDR) for three days (D3). Then, cells were transferred to Dulbecco’s modified Eagle’s medium with rosiglitazone and re-fed every two days. Hcy (0, 0.05, 0.1 mmol/L) were added from D0 and refreshed with the medium. Mutation of 3T3-L1 adipocytes was determined by Oil Red O staining and the intracellular triglyceride (TG) assay on day 7. Fully differentiated cells were stained with Hoechest 33342 and counted with a hemocytometer. The total mRNA was isolated to determine the gene expression of peroxisome proliferator-activated receptor gamma (PPAR-gamma) and adipocyte protein 2 (AP2) via realtime reverse transcription polymerase chain reaction. (a, b) Hcy reduced intracellular TG concentrations; (a, c) Hcy reduced cell number. Gene expressions of both PPAR-gamma (d) and AP2 (e) were suppressed. Data are means ± SD (n = 3). *P < 0.05 compared with the MDR-induced Group (Rosi). Rosi, rosiglitazone. (A color version of this figure is available in the online journal)