title: Liquiritin attenuates advanced glycation end products-induced endothelial dysfunction via RAGE/NF-κB pathway in human umbilical vein endothelial cells.
abstract: Advanced glycation end products (AGEs)-induced vasculopathy, including oxidative stress, inflammation and apoptosis responses, contributes to the high morbidity and mortality of coronary artery diseases in diabetic patients. The present study was conducted to evaluate the protective activity of liquiritin (Liq) on AGEs-induced endothelial dysfunction and explore its underlying mechanisms. After pretreatment with Liq, a significant reduction in AGEs-induced apoptosis, as well as reactive oxygen species generation and malondialdehyde level in human umbilical vein endothelial cells (HUVECs) were observed via acridine orange/ethidium bromide fluorescence staining test. Notably, Liq also significantly increased AGEs-reduced superoxide dismutase activity. Furthermore, the pretreatment with receptor for advanced glycation end products (RAGE)-antibody or Liq remarkably down-regulated TGF-beta1 and RAGE protein expressions and significantly blocked NF-κB activation which were proved by immunocytochemistry or immunofluorescence assays. These results indicated that Liq held potential for the protection on AGEs-induced endothelial dysfunction via RAGE/NF-κB pathway in HUVECs and might be a promising agent for the treatment of vasculopathy in diabetic patients.
authors.affiliation: School of Pharmacy, Xinxiang Medical University, Xinxiang, 453003, Henan, People's Republic of China.
authors.forename: Xiaoyi
authors.initials: X
authors.lastname: Zhang
authors.forename: Yu
authors.initials: Y
authors.lastname: Song
authors.forename: Xiaolin
authors.initials: X
authors.lastname: Han
authors.forename: Liang
authors.initials: L
authors.lastname: Feng
authors.forename: Rushang
authors.initials: R
authors.lastname: Wang
authors.forename: Minghua
authors.initials: M
authors.lastname: Zhang
authors.forename: Maomao
authors.initials: M
authors.lastname: Zhu
authors.forename: Xiaobin
authors.initials: X
authors.lastname: Jia
authors.forename: Shaoying
authors.initials: S
authors.lastname: Hu
mesh_terms: D000911:Antibodies, Monoclonal; D017209:Apoptosis / Q000187:drug effects; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000378:metabolism; D015536:Down-Regulation; D044950:Flavanones / Q000494:pharmacology*; D005960:Glucosides / Q000494:pharmacology*; D017127:Glycation End Products, Advanced / Q000276:immunology / Q000378:metabolism*; D029001:Herbal Medicine; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D008315:Malondialdehyde / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D000067759:Receptor for Advanced Glycation End Products / Q000096:biosynthesis / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D013482:Superoxide Dismutase / Q000187:drug effects / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis
chemical_list: D000911:Antibodies, Monoclonal; D044950:Flavanones; D005960:Glucosides; D017127:Glycation End Products, Advanced; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D000067759:Receptor for Advanced Glycation End Products; D053773:Transforming Growth Factor beta1; D008315:Malondialdehyde; D013482:Superoxide Dismutase; C512196:liquiritin