2. Academic Validation
  3. Agrimol B suppresses adipogenesis through modulation of SIRT1-PPAR gamma signal pathway

Agrimol B suppresses adipogenesis through modulation of SIRT1-PPAR gamma signal pathway

  • Biochem Biophys Res Commun. 2016 Aug 26;477(3):454-60. doi: 10.1016/j.bbrc.2016.06.078.
Shifeng Wang 1,  Qiao Zhang 1,  Yuxin Zhang 1,  Cheng Shen 1,  Zhen Wang 2,  Qinghua Wu 3,  Yanling Zhang 1,  Shiyou Li 4,  Yanjiang Qiao 5
Affiliations

Affiliations

  • 1 School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100102, China.
  • 2 Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China.
  • 3 HD Biosciences Co., Ltd, Shanghai 201201, China.
  • 4 Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China. Electronic address: lishiyou@big.ac.cn.
  • 5 School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100102, China. Electronic address: yjqiao@bucm.edu.cn.
PMID: 27320865 DOI: 10.1016/j.bbrc.2016.06.078
Abstract

Studies of human genetics have implicated the role of SIRT1 in regulating obesity, Insulin resistance, and longevity. These researches motivated the identification of novel SIRT1 activators. The current study aimed to investigate the potential efficacy of agrimol B, a polyphenol derived from Agrimonia pilosa Ledeb., on mediating SIRT1 activity and fat metabolism. Results showed that agrimol B significantly induced cytoplasm-to-nucleus shuttle of SIRT1. Furthermore, we confirmed that agrimol B dramatically inhibited 3T3-L1 adipocyte differentiation by reducing PPARγ, C/EBPα, FAS, UCP-1, and apoE expression. Consequently, adipogenesis was blocked by treatment of agrimol B at the early stage of differentiation in a dose-dependent manner, the IC50 value was determined as 3.35 ± 0.32 μM. Taken together, our data suggest a therapeutic potential of agrimol B on alleviating obesity, through modulation of SIRT1-PPARγ signal pathway.

Keywords

Agrimol B; Agrimonia pilosa Ledeb.; Lipid droplet; Obesity; PPARγ; SIRT1.

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