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Epigallocatechin‐3‐gallate suppresses the lipid deposition through the apoptosis during differentiation in bovine bone marrow mesenchymal stem cells
Author(s) -
Jeong Jin Young,
Suresh Sekar,
Jang Mi,
Park Mi Na,
Gobianand Kuppannan,
You Seungkwon,
Yeon SungHeom,
Lee HyunJeong
Publication year - 2015
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10343
Subject(s) - adipogenesis , terminal deoxynucleotidyl transferase , peroxisome proliferator activated receptor gamma , mesenchymal stem cell , microbiology and biotechnology , apoptosis , biology , tunel assay , stem cell , chemistry , peroxisome proliferator activated receptor , biochemistry , receptor
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.