Rubrofusarin-6-β-gentiobioside inhibits lipid accumulation and weight gain by regulating AMPK/mTOR signaling.
3T3-L1 Cells
AMP-Activated Protein Kinases
/ metabolism
Adipocytes
/ drug effects
Adipogenesis
/ drug effects
Animals
Anti-Obesity Agents
/ pharmacology
Body Weight
/ drug effects
Chromones
/ pharmacology
Diet, High-Fat
/ adverse effects
Glucosides
/ pharmacology
Humans
Lipid Metabolism
/ drug effects
Male
Mesenchymal Stem Cells
/ drug effects
Mice
Mice, Obese
Obesity
/ drug therapy
TOR Serine-Threonine Kinases
/ metabolism
Weight Gain
/ drug effects
3T3-L1
AMPK
Cassiae tora seed
Human adipose mesenchymal stem cells
Rubrofusarin-6-β-gentiobioside
mTOR
Journal
Phytomedicine : international journal of phytotherapy and phytopharmacology
ISSN: 1618-095X
Titre abrégé: Phytomedicine
Pays: Germany
ID NLM: 9438794
Informations de publication
Date de publication:
Sep 2019
Sep 2019
Historique:
received:
23
07
2018
revised:
06
05
2019
accepted:
08
05
2019
pubmed:
28
5
2019
medline:
28
2
2020
entrez:
28
5
2019
Statut:
ppublish
Résumé
Although rubrofusarin-6-β-gentiobioside (RFG), which is a component of Cassiae tora seed, could likely regulate hyperlipidemia, its anti-obesity effect and related mechanism have not been elucidated. The aim of this study was to examine whether RFG can ameliorate obesity and the mechanism of lipid accumulation regulated by RFG. In in vitro experiments, we confirmed the anti-adipogenic effect of RFG using 3T3-L1 cells and human adipose mesenchymal stem cells (hAMSCs). To confirm the anti-obesity effect, High-Fat Diet (HFD)-induced obese mice were selected as a model. We investigated anti-adipogenic effects of RFG using MTS assay, Oil Red O Staining, real-time RT-PCR, western blot analysis, and immunofluorescence staining. The anti-obesity effect of RFG was confirmed in HFD-induced mice model using hematoxylin and eosin staining and serum analysis. RFG inhibited lipid accumulation in 3T3-L1 cells and hAMSCs by reducing expression of mammalian targets of rapamycin (mTOR), peroxisome proliferator-activated receptor (PPAR)γ, and CCAAT-enhancer binding protein (C/EBP)α. RFG phosphorylated AMP-activated protein kinase (AMPK) in a liver kinase B (LKB) 1-independent manner. Moreover, the anti-adipogenic effect of RFG was blocked by AMPK inhibitor. These results suggest that RFG inhibits lipid accumulation via AMPK signaling. Furthermore, RFG reduced the body weight, size of epididymal white adipose tissue (eWAT), and fatty liver in the mice. RFG also suppressed levels of adipogenic factors PPARγ, C/EBPα, FAS, LPL, and aP2) by activating AMPK in the eWAT and liver. RFG can ameliorate obesity, and thus, could be used as a therapeutic agent for treating obesity.
Sections du résumé
BACKGROUND
BACKGROUND
Although rubrofusarin-6-β-gentiobioside (RFG), which is a component of Cassiae tora seed, could likely regulate hyperlipidemia, its anti-obesity effect and related mechanism have not been elucidated.
PURPOSE
OBJECTIVE
The aim of this study was to examine whether RFG can ameliorate obesity and the mechanism of lipid accumulation regulated by RFG.
STUDY DESIGN
METHODS
In in vitro experiments, we confirmed the anti-adipogenic effect of RFG using 3T3-L1 cells and human adipose mesenchymal stem cells (hAMSCs). To confirm the anti-obesity effect, High-Fat Diet (HFD)-induced obese mice were selected as a model.
METHODS
METHODS
We investigated anti-adipogenic effects of RFG using MTS assay, Oil Red O Staining, real-time RT-PCR, western blot analysis, and immunofluorescence staining. The anti-obesity effect of RFG was confirmed in HFD-induced mice model using hematoxylin and eosin staining and serum analysis.
RESULTS
RESULTS
RFG inhibited lipid accumulation in 3T3-L1 cells and hAMSCs by reducing expression of mammalian targets of rapamycin (mTOR), peroxisome proliferator-activated receptor (PPAR)γ, and CCAAT-enhancer binding protein (C/EBP)α. RFG phosphorylated AMP-activated protein kinase (AMPK) in a liver kinase B (LKB) 1-independent manner. Moreover, the anti-adipogenic effect of RFG was blocked by AMPK inhibitor. These results suggest that RFG inhibits lipid accumulation via AMPK signaling. Furthermore, RFG reduced the body weight, size of epididymal white adipose tissue (eWAT), and fatty liver in the mice. RFG also suppressed levels of adipogenic factors PPARγ, C/EBPα, FAS, LPL, and aP2) by activating AMPK in the eWAT and liver.
CONCLUSION
CONCLUSIONS
RFG can ameliorate obesity, and thus, could be used as a therapeutic agent for treating obesity.
Identifiants
pubmed: 31132754
pii: S0944-7113(19)30121-7
doi: 10.1016/j.phymed.2019.152952
pii:
doi:
Substances chimiques
Anti-Obesity Agents
0
Chromones
0
Glucosides
0
rubrofusarin gentiobioside
0
TOR Serine-Threonine Kinases
EC 2.7.11.1
AMP-Activated Protein Kinases
EC 2.7.11.31
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
152952Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier GmbH.. All rights reserved.