Inhibitory Effects of Bojungchiseub-tang on Adipocyte Differentiation and Adipogenesis in 3T3-L1 Preadipocytes

보중치습탕이 3T3-L1 지방전구세포의 분화 및 지방생성 억제에 미치는 영향

  • Lee, Soo Jung (Department of Internal Medicine, College of Korean Medicine, Dong-Eui University) ;
  • Kim, Won Il (Department of Internal Medicine, College of Korean Medicine, Dong-Eui University) ;
  • Kang, Kyung Hwa (Department of Physiology, College of Korean Medicine, Dong-Eui University)
  • 이수정 (동의대학교 한의과대학 비계내과학교실) ;
  • 김원일 (동의대학교 한의과대학 비계내과학교실) ;
  • 강경화 (동의대학교 한의과대학 생리학교실)
  • Received : 2014.04.24
  • Accepted : 2014.06.12
  • Published : 2014.06.25

Abstract

Bojungchiseub-tang (BJCST) has been used in symptoms and signs of edema, dampness-phlegm, kidney failure, and so on. BJCST is also expected to have strong anti-obesity activities. However, little is known about the mechanisms of its inhibitory effects on adipocyte differentiation and adipogenesis. In the present study, we examined the effects and mechanism of BJCST on transcription factors and adipogenic genes of 3T3-L1 preadipocytes to understand its inhibitory effects on adipocyte differentiation and adipogenesis. Our results showed that BJCST significantly inhibited differentiation and adipogenesis of 3T3-L1 preadipocytes in a dose-dependent manner. To elucidate the mechanism of the effects of BJCST on lowering lipid content in 3T3-L1 adipocytes, we examined whether BJCST modulate the expressions of transcription factors to induce adipogenesis and adipogenic genes related to regulate accumulation of lipids. As a result, the expression of steroid regulatory element-binding protein (SREBP)1, cytidine-cytidine-adenosine-adenosine-thymidine (CCAAT)/enhancer binding proteins ${\alpha}$ ($C/EBP{\alpha}$), $C/EBP{\beta}$, $C/EBP{\delta}$, and peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$) genes, which induce the adipose differentiation, liver X receptor $(LXR){\alpha}$ and fatty acid synthase (FAS) genes, which induce lipogenesis and adipose-specific aP2, Adipsin, lipoprotein lipase (LPL), CD36, TGF-${\beta}$, leptin and adiponectin genes, which compose fat formation were decreased. BJCST also reduced the expression of acyl CoA oxidase (ACO) and uncoupling protein (UCP) genes related to lipid oxidation. In conclusion, BJCST could regulate transcript factor related to induction of adipose differentiation and inhibited the accumulation of lipids and expression of adipogenic genes.

Keywords

References

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