title: Quercetin alleviates cell apoptosis and inflammation via the ER stress pathway in vascular endothelial cells cultured in high concentrations of glucosamine.
abstract: Glucosamine is a possible cause of vascular endothelial injury in the initial stages of atherosclerosis, through endoplasmic reticulum (ER) stress resulting in fatty streaks in the vascular wall. Quercetin is an anti‑diabetic and cardiovascular protective agent that has previously been demonstrated to reduce ER stress in human umbilical vein endothelial cells (HUVECs). The present study aimed to investigate whether quercetin prevents glucosamine‑induced apoptosis and inflammation via ER stress pathway in HUVECs. The effect of quercetin on cell viability, apoptosis, and protein expression levels of inflammatory cytokines and ER stress markers was investigated in glucosamine‑supplemented HUVECs. Quercetin was demonstrated to protect against glucosamine‑induced apoptosis, improved cell viability, and inhibited expression of pro‑inflammatory factors and endothelin‑1. Quercetin treatment also reduced the expression levels of glucose‑regulated protein 78, phosphorylated protein kinase‑like ER kinase, phosphorylated c‑Jun N‑terminal kinase and C/EBP homologous protein. In conclusion, quercetin may have auxiliary therapeutic potential against glucosamine‑induced cell apoptosis and inflammation, which may be partially due to alleviation of ER stress.
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing 100191, P.R. China.
authors.forename: Xiaxia
authors.initials: X
authors.lastname: Cai
authors.affiliation: Department of Clinical Nutrition, Peking University International Hospital, Beijing 100191, P.R. China.
authors.forename: Lei
authors.initials: L
authors.lastname: Bao
authors.affiliation: Department of Maternal, Child and Adolescent Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, P.R. China.
authors.forename: Ye
authors.initials: Y
authors.lastname: Ding
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing 100191, P.R. China.
authors.forename: Xiaoqian
authors.initials: X
authors.lastname: Dai
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing 100191, P.R. China.
authors.forename: Zhaofeng
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing 100191, P.R. China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Li
mesh_terms: D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects; D000091342:Endoplasmic Reticulum Chaperone BiP; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D019332:Endothelin-1 / Q000032:analysis; D004797:Enzyme-Linked Immunosorbent Assay; D005944:Glucosamine / Q000633:toxicity*; D006360:Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D007249:Inflammation / Q000517:prevention & control; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D011794:Quercetin / Q000494:pharmacology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis
chemical_list: D000975:Antioxidants; D022762:CCAAT-Enhancer-Binding Proteins; D016207:Cytokines; D000091342:Endoplasmic Reticulum Chaperone BiP; D019332:Endothelin-1; D006360:Heat-Shock Proteins; C573420:ICAM1 protein, human; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D011794:Quercetin; D048031:JNK Mitogen-Activated Protein Kinases; D005944:Glucosamine