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Cichoric Acid Reverses Insulin Resistance and Suppresses Inflammatory Responses in the Glucosamine-Induced HepG2 Cells.

Abstract
Cichoric acid, a caffeic acid derivative found in Echinacea purpurea, basil, and chicory, has been reported to have bioactive effects, such as anti-inflammatory, antioxidant, and preventing insulin resistance. In this study, to explore the effects of CA on regulating insulin resistance and chronic inflammatory responses, the insulin resistance model was constructed by glucosamine in HepG2 cells. CA stimulated glucosamine-mediated glucose uptake by stimulating translocation of the glucose transporter 2. Moreover, the production of reactive oxygen, the expression of COX-2 and iNOS, and the mRNA levels of TNF-α and IL-6 were attenuated. Furthermore, CA was verified to promote glucosamine-mediated glucose uptake and inhibited inflammation through PI3K/Akt, NF-κB, and MAPK signaling pathways in HepG2 cells. These results implied that CA could increase glucose uptake, improve insulin resistance, and attenuate glucosamine-induced inflammation, suggesting that CA is a potential natural nutraceutical with antidiabetic properties and anti-inflammatory effects.
AuthorsDi Zhu, Yutang Wang, Qingwei Du, Zhigang Liu, Xuebo Liu
JournalJournal of agricultural and food chemistry (J Agric Food Chem) Vol. 63 Issue 51 Pg. 10903-13 (Dec 30 2015) ISSN: 1520-5118 [Electronic] United States
PMID26592089 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Anti-Inflammatory Agents
  • Caffeic Acids
  • Glucose Transporter Type 2
  • Hypoglycemic Agents
  • Succinates
  • Glucose
  • Glucosamine
  • chicoric acid
Topics
  • Anti-Inflammatory Agents
  • Caffeic Acids (pharmacology)
  • Dietary Supplements
  • Glucosamine (pharmacology)
  • Glucose (metabolism)
  • Glucose Transporter Type 2 (drug effects, metabolism)
  • Hep G2 Cells
  • Humans
  • Hypoglycemic Agents
  • Inflammation (chemically induced, prevention & control)
  • Insulin Resistance
  • Liver (drug effects, metabolism)
  • Signal Transduction (drug effects)
  • Succinates (pharmacology)

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