3,5-Dicaffeoyl-Epi-Quinic Acid Isolated from Edible Halophyte Atriplex gmelinii Inhibits Adipogenesis via AMPK/MAPK Pathway in 3T3-L1 Adipocytes.
Jung Hwan OhJung Im LeeFatih KaradenizYoungwan SeoChang-Suk KongPublished in: Evidence-based complementary and alternative medicine : eCAM (2018)
Atriplex gmelinii is an edible halophyte that has been suggested to possess various health benefits. In the present study, 3,5-dicaffeoyl-epi-quinic acid (DEQA) isolated from A. gmelinii was tested for its ability to prevent adipogenesis in 3T3-L1 cells. Also, the molecular mechanisms by which DEQA affects differentiation of 3T3-L1 cells were investigated. The introduction of DEQA to differentiating 3T3-L1 preadipocytes resulted in suppressed adipogenesis and lowered expression of adipogenesis-related factors, PPARγ, C/EBPα, and SREBP-1c. Treatment of 3T3-L1 adipocytes with DEQA notably decreased the levels of phosphorylated p38, ERK, and JNK. In addition, presence of DEQA upregulated the levels of both inactive and phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and its substrate, acetyl-CoA carboxylase (ACC). Taken together, current results indicated that DEQA exhibited a significant antiadipogenesis activity by activation of AMPK and downregulation of MAPK signal pathways in 3T3-L1 preadipocytes.
Keyphrases
- signaling pathway
- induced apoptosis
- protein kinase
- high fat diet induced
- pi k akt
- cell cycle arrest
- oxidative stress
- skeletal muscle
- adipose tissue
- healthcare
- endoplasmic reticulum stress
- insulin resistance
- cell proliferation
- cell death
- poor prognosis
- mental health
- magnetic resonance imaging
- metabolic syndrome
- computed tomography
- climate change
- atomic force microscopy
- contrast enhanced
- health information
- binding protein
- high speed
- risk assessment
- combination therapy
- smoking cessation