Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury

Chin J Integr Med. 2016 Jan;22(1):36-41. doi: 10.1007/s11655-015-1976-x. Epub 2015 May 27.

Abstract

Objective: This study observed attenuating effect of hydroxysafflor yellow A (HSYA), an effective ingredient of aqueous extract of Carthamus tinctorius L, on lipopolysaccharide (LPS)-induced endothelium inflammatory injury.

Methods: Eahy926 human endothelium cell (EC) line was used; thiazolyl blue tetrazolium bromide (MTT) test was assayed to observe the viability of EC; Luciferase reporter gene assay was applied to measure nuclear factor-κB (NF-κB) p65 subunit nuclear binding activity in EC; Western blot technology was used to monitor mitogen activated protein kinase (MAPKs) and NF-κB activation. Reverse transcription polymerase chain reaction (RT-PCR) method was applied to observe intercellular cell adhesion molecule-1 (ICAM-1) and E-selectin mRNA level; EC surface ICAM-1 expression was measured with flow cytometry and leukocyte adhesion to EC was assayed with Rose Bengal spectrophotometry technology.

Results: HSYA protected EC viability against LPS-induced injury (P <0.05). LPS-induced NF-κB p65 subunit DNA binding (P <0.01) and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor α (IκBα) phosphorylation was inhibited by HSYA. HSYA attenuated LPS triggered ICAM-1 and E-selectin mRNA levels elevation and phosphorylation of p38 MAPK or c-Jun N-terminal kinase MAPK. HSYA also inhibited LPS-induced cell surface ICAM-1 protein expression P <0.01) and leukocyte adhesion to EC (P <0.05).

Conclusion: HSYA is effective to protect LPS-induced high expression of endothelium adhesive molecule and inflammatory signal transduction.

Keywords: adhesive molecule; endothelium cell; hydroxysafflor yellow A; inflammation; lipopolysaccharide.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Adhesion / drug effects
  • Cell Nucleus / drug effects
  • Cell Nucleus / metabolism
  • Cell Survival / drug effects
  • Chalcone / analogs & derivatives*
  • Chalcone / chemistry
  • Chalcone / pharmacology
  • Chalcone / therapeutic use
  • E-Selectin / genetics
  • E-Selectin / metabolism
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / pathology*
  • Gene Expression Regulation / drug effects
  • Human Umbilical Vein Endothelial Cells / drug effects
  • Human Umbilical Vein Endothelial Cells / metabolism
  • Human Umbilical Vein Endothelial Cells / pathology
  • Humans
  • I-kappa B Proteins / metabolism
  • Inflammation / drug therapy*
  • Inflammation / pathology
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Leukocytes / cytology
  • Leukocytes / drug effects
  • Lipopolysaccharides
  • MAP Kinase Signaling System / drug effects
  • NF-KappaB Inhibitor alpha
  • Phosphorylation / drug effects
  • Protective Agents / pharmacology
  • Protein Binding / drug effects
  • Quinones / chemistry
  • Quinones / pharmacology*
  • Quinones / therapeutic use*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism

Substances

  • E-Selectin
  • I-kappa B Proteins
  • Lipopolysaccharides
  • NFKBIA protein, human
  • Protective Agents
  • Quinones
  • RNA, Messenger
  • Intercellular Adhesion Molecule-1
  • NF-KappaB Inhibitor alpha
  • hydroxysafflor yellow A
  • Chalcone