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- Title
Epigallocatechin-3-gallate suppresses the lipid deposition through the apoptosis during differentiation in bovine bone marrow mesenchymal stem cells.
- Authors
Jeong, Jin Young; Suresh, Sekar; Jang, Mi; Park, Mi Na; Gobianand, Kuppannan; You, Seungkwon; Yeon, Sung‐Heom; Lee, Hyun‐Jeong
- Abstract
Epigallocatechin gallate (EGCG), a major component of tea, has known effects on obesity, fatty liver, and obesity-related cancer. We explored the effects of EGCG on the differentiation of bovine mesenchymal stem cells (BMSCs, which are multipotent) in a dose- and time-dependent manner. Differentiating BMSCs were exposed to various concentrations of EGCG (0, 10, 50, 100, and 200 µM) for 2, 4, and 6 days. BMSCs were cultured in Dulbecco's modified Eagle's medium (DMEM)/high-glucose medium with adipogenic inducers for 6 days, and the expression levels of various genes involved in adipogenesis were measured using real-time polymerase chain reaction (PCR) and Western blotting. We assessed apoptosis by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining of control and EGCG-exposed cells. We found that EGCG significantly suppressed fat deposition and cell viability ( P < 0.05). The mRNA and protein levels of various adipogenic factors were measured. Expression of the genes encoding peroxisome proliferator-activated receptor gamma (PPARG), CCAAT/enhancer-binding protein alpha (CEBPA), fatty acid-binding protein 4 (FABP4), and stearoyl-CoA desaturase (SCD) were diminished by EGCG during adipogenic differentiation ( P < 0.05). We also found that EGCG lowered the expression levels of the adipogenic proteins encoded by these genes ( P < 0.05). EGCG induced apoptosis during adipogenic differentiation ( P < 0.05). Thus, exposure to EGCG potentially inhibits adipogenesis by triggering apoptosis; the data suggest that EGCG inhibits adipogenic differentiation in BMSCs.
- Subjects
EPIGALLOCATECHIN gallate; OBESITY; CANCER risk factors; MESENCHYMAL stem cells; BOS; PEROXISOMES
- Publication
Cell Biology International, 2015, Vol 39, Issue 1, p52
- ISSN
1065-6995
- Publication type
Article
- DOI
10.1002/cbin.10343