Ellagic Acid Reduces Adipogenesis through Inhibition of Differentiation-Prevention of the Induction of Rb Phosphorylation in 3T3-L1 Adipocytes
Authors: Ye Wang
Xiaoli Ma
Jun Ren
Xinjian Ran
Lifeng Wang
Xin Luo
Upur Halmurati
Xinmin Mao
Mei Long
Yicun Tao
Minfang Zhang
Linlin Li
Journal: Evidence-based Complementary and Alternative Medicine (2013)
Discipline: CLINICAL MEDICINE
Keywords: Ellagic acid; adipogenesis; 3T3-L1 preadipocytes; lipid droplets; cell cycle
Affiliations: Department of Physiology, Preclinical School, Xinjiang Medical University, Urumqi, Xinjiang 830011, China., Department of Pharmacology, School of Pharmacy, Xinjiang Medical University, Urumqi, Xinjiang 830011, China, Lab Center of Mechanism, Preclinical School, Xinjiang Medical University, Urumqi, Xinjiang 830011, China, Electron Microscopy Center, Key Laboratory of Endemic Disease, Xinjiang Medical University, Urumqi, Xinjiang 830011, China, Analytical & Testing Center, School of Pharmacy, Xinjiang Medical University, Urumqi, Xinjiang 830011, China, Xinjiang Medical University, Urumqi, Xinjiang 830011, China, School of Traditional Chinese Medicine, Xinjiang Medical University, Urumqi, Xinjiang 830011, China, Pharmacy School, Xinjiang Medical University, Urumqi, Xinjiang 830000, China, Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA

Abstract:  Ellagic acid (EA) present in many fruits and nuts serves as antiproliferation, anti-inflammatory, and antitumorigenic properties. However, the effect of EA on preadipocytes adipogenesis and its mechanism(s) have not been elucidated. The present study was designed to examine the effect of EA on adipogenesis in 3T3-L1 preadipocytes and underlying mechanism(s) of action involved. Data show that EA administration decreased the accumulation of lipid droplets. The inhibition was diminished when the addition of EA was delayed to days 2-4 of differentiation. Clonal expansion was reduced in the presence of EA. FACS analysis showed that EA blocked the cell cycle at the G1/S transition. EdU incorporation also confirmed that EA refrained cell from entering S phase. Our data also revealed that the differentiation-induced protein expression of Cyclin A and phosphorylation of the retinoblastoma protein (Rb) were impaired by EA. Differentiation-dependent expression and DNA-binding ability of C/EBP Œ± were also inhibited by EA. Alterations in cell cycle-associated proteins may be important with respect to the antiadipogenic action of EA. In conclusion, EA is capable of inhibiting adipogenesis in 3T3-L1 adipocytes possibly through reduction of Cyclin A protein expression and Rb phosphorylation. With the blocking of G1/S phase transition, EA suppresses terminal differentiation and lipid accumulation in 3T3-L1 adipocytes. 

Retracted: No

PubPeer comments:
 image duplications  Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,