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Fucosterol protects cobalt chloride induced inflammation by the inhibition of hypoxia-inducible factor through PI3K/Akt pathway.

Abstract
Fucosterol is a phytosterol commonly extracted from algae. It has been proved that fucosterol possesses antioxidant activity that is capable of scavenging the free radicals causing skin damages. In this study, we investigated the protective mechanisms of fucosterol on cobalt chloride (CoCl2) induced hypoxia damages to keratinocytes (HaCaT). We found that fucosterol inhibited CoCl2 induced cytotoxicity and inflammation in a dose-dependent manner. Furthermore, fucosterol attenuated CoCl2 induced excess expression of IL-6, IL-1β and TNF-α in HaCaT cells. In addition, fucosterol surpressed the phosphorylation of PI3K and Akt and accumulation of HIF1-α simulated by CoCl2. Taken together, these results suggested that fucosterol executed its protective effects against CoCl2 induced cytotoxicity and inflammation by the inhibition of hypoxia inducible factor through PI3K/Akt pathway.
AuthorsZhengwang Sun, Mohamed Antar Aziz Mohamed, Sang Yong Park, Tae Hoo Yi
JournalInternational immunopharmacology (Int Immunopharmacol) Vol. 29 Issue 2 Pg. 642-647 (Dec 2015) ISSN: 1878-1705 [Electronic] Netherlands
PMID26395918 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2015 Elsevier B.V. All rights reserved.
Chemical References
  • Chromones
  • Cytokines
  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Morpholines
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Cobalt
  • fucosterol
  • Stigmasterol
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • cobaltous chloride
Topics
  • Cell Line
  • Chromones (pharmacology)
  • Cobalt (toxicity)
  • Cytokines (genetics, metabolism)
  • Gene Expression Regulation (drug effects)
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit (antagonists & inhibitors, genetics, metabolism)
  • Inflammation (chemically induced, prevention & control)
  • Keratinocytes (drug effects)
  • Morpholines (pharmacology)
  • Phosphatidylinositol 3-Kinases (genetics, metabolism)
  • Phosphorylation
  • Proto-Oncogene Proteins c-akt (genetics, metabolism)
  • Stigmasterol (analogs & derivatives, pharmacology)

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