Open AccessSynthesis and cardiovascular protective effects of quercetin 7‐O‐sialic acid
Author(s) -
Tian Hua,
Liu Qingchao,
Qin Shucun,
Zong Chuanlong,
Zhang Ying,
Yao Shutong,
Yang Nana,
Guan Tao,
Guo Shoudong
Publication year - 2017
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12943
Subject(s) - oxidative stress , chemistry , reactive oxygen species , inflammation , biochemistry , lipoprotein , tumor necrosis factor alpha , high density lipoprotein , sialic acid , cholesterol , pharmacology , immunology , biology
Oxidative stress and inflammation play important roles in the pathogenesis of cardiovascular disease ( CVD ). Oxidative stress‐induced desialylation is considered to be a primary step in atherogenic modification, and therefore, the attenuation of oxidative stress and/or inflammatory reactions may ameliorate CVD . In this study, quercetin 7‐O‐sialic acid ( QA ) was synthesized aiming to put together the cardiovascular protective effect of quercetin and the recently reported anti‐oxidant and anti‐atherosclerosis functions of N ‐acetylneuraminic acid. The biological efficacy of QA was evaluated in vitro in various cellular models. The results demonstrated that 50 μM QA could effectively protect human umbilical vein endothelial cells ( HUVEC , EA .hy926) against hydrogen peroxide‐ or oxidized low‐density lipoprotein‐induced oxidative damage by reducing the production of reactive oxygen species. QA attenuated hydrogen peroxide‐induced desialylation of HUVEC and lipoproteins. QA decreased lipopolysaccharide‐induced secretion of tumour necrosis factor‐α ( TNF ‐α) and monocyte chemoattractant protein‐1 ( MCP ‐1), and it significantly reduced the expression of intercellular adhesion molecule‐1, vascular cell adhesion molecule‐1, TNF ‐α and MCP ‐1. Furthermore, QA effectively promoted cholesterol efflux from Raw 264.7 macrophages to apolipoprotein A‐1 and high‐density lipoprotein by up‐regulating ATP ‐binding cassette transporter A1 and G1, respectively. Results indicated that the novel compound QA exhibited a better capacity than quercetin for anti‐oxidation, anti‐inflammation, cholesterol efflux promotion and biomolecule protection against desialylation and therefore could be a candidate compound for the prevention or treatment of CVD .