- Author:
Ming JIN
1
;
Chun-Yan SUN
2
;
Bao-Xia ZANG
2
Author Information
- Publication Type:Journal Article
- Keywords: adhesive molecule; endothelium cell; hydroxysafflor yellow A; inflammation; lipopolysaccharide
- MeSH: Cell Adhesion; drug effects; Cell Nucleus; drug effects; metabolism; Cell Survival; drug effects; Chalcone; analogs & derivatives; chemistry; pharmacology; therapeutic use; E-Selectin; genetics; metabolism; Endothelium, Vascular; drug effects; pathology; Gene Expression Regulation; drug effects; Human Umbilical Vein Endothelial Cells; drug effects; metabolism; pathology; Humans; I-kappa B Proteins; metabolism; Inflammation; drug therapy; pathology; Intercellular Adhesion Molecule-1; genetics; metabolism; Leukocytes; cytology; 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; pharmacology; therapeutic use; RNA, Messenger; genetics; metabolism
- From: Chinese journal of integrative medicine 2016;22(1):36-41
- CountryChina
- Language:English
-
Abstract:
OBJECTIVEThis 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.
METHODSEahy926 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.
RESULTSHSYA 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).
CONCLUSIONHSYA is effective to protect LPS-induced high expression of endothelium adhesive molecule and inflammatory signal transduction.