Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury
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Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury
Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury
中国结合医学杂志(英文版)2016年22卷第1期 页码:36-41
Affiliations:
Department of Pharmacology, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University,Beijing,China
Author bio:
Funds:
Supported by National Natural Science Foundation of China (No. 81270103) and Natural Science Foundation of Beijing (No. 7102025)
Jin, M., Sun, Cy. & Zang, Bx. Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury., Chin. J. Integr. Med. 22, 36–41 (2016). https://doi.org/10.1007/s11655-015-1976-x
Ming Jin, Chun-yan Sun, Bao-xia Zang. Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury[J]. Chinese Journal of Integrative Medicine, 2016,22(1):36-41.
Jin, M., Sun, Cy. & Zang, Bx. Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury., Chin. J. Integr. Med. 22, 36–41 (2016). https://doi.org/10.1007/s11655-015-1976-xDOI:
Ming Jin, Chun-yan Sun, Bao-xia Zang. Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury[J]. Chinese Journal of Integrative Medicine, 2016,22(1):36-41. DOI: 10.1007/s11655-015-1976-x.
Hydroxysafflor yellow A attenuate lipopolysaccharide-induced endothelium inflammatory injury
摘要
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. 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. 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). HSYA is effective to protect LPS-induced high expression of endothelium adhesive molecule and inflammatory signal transduction.
Abstract
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. 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. 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). HSYA is effective to protect LPS-induced high expression of endothelium adhesive molecule and inflammatory signal transduction.
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