1. Academic Validation
  2. Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury

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.
Ming Jin 1 Chun-Yan Sun 2 Bao-Xia Zang 2
Affiliations

Affiliations

  • 1 Department of Pharmacology, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, Beijing, 100029, China. jm64456308@163.com.
  • 2 Department of Pharmacology, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, Beijing, 100029, China.
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.

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