title: Protective effects of isorhamnetin on apoptosis and inflammation in TNF-α-induced HUVECs injury.
abstract: Little is known about the role of isorhamnetin on endothelial cell apoptosis and inflammation when insulted by TNF-α injury. In our study, HUVECs were treated with TNF-α for 6 hours. HUVECs apoptosis were detected using flow cytometry. The expressions of ICAM-1, VCAM-1, E-selectin, NF-κB, AP-1 and eNOS were determined with western blotting or flow cytometry. The results showed TNF-α increased of apoptosis and the expression of ICAM-1, VCAM-1 and E-selectin in HUVECs, accompanied by significant augmentation of NF-κB and AP-1 expression. Pretreatment with isorhamnetin significantly reduced apoptosis in TNF-α-treated HUVECs. Moreover, isorhamnetin significantly attenuated TNF-α-induced upregulation of ICAM-1, VCAM-1, AP-1, E-selectin and NF-κB expression. Meanwhile, isorhamnetin also increased the expression of eNOS. So, isorhamnetin could suppress TNF-α-induced apoptosis and inflammation by blocking NF-κB and AP-1 signaling in HUVECs, which might be one of the underlying mechanisms for treatment of coronary heart disease.
authors.affiliation: Department of Cardiology, Hangzhou Hospital of TCM 453 Ti Yu Chang Road, Hangzhou 310007, China.
authors.forename: Tie-Long
authors.initials: TL
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Hangzhou Hospital of TCM 453 Ti Yu Chang Road, Hangzhou 310007, China.
authors.forename: Guang-Li
authors.initials: GL
authors.lastname: Zhu
authors.affiliation: Department of Cardiology, The Second Affiliated Hospital, College of Medicine, Zhejiang University 88 Fang Road, Hangzhou 310009, China.
authors.forename: Jian-An
authors.initials: JA
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Hangzhou Hospital of TCM 453 Ti Yu Chang Road, Hangzhou 310007, China.
authors.forename: Guo-Dong
authors.initials: GD
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, Hangzhou Hospital of TCM 453 Ti Yu Chang Road, Hangzhou 310007, China.
authors.forename: Hong-Fei
authors.initials: HF
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Hangzhou Hospital of TCM 453 Ti Yu Chang Road, Hangzhou 310007, China.
authors.forename: Jin-Ru
authors.initials: JR
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Hangzhou Hospital of TCM 453 Ti Yu Chang Road, Hangzhou 310007, China ; Zhejiang University of TCM Hangzhou 310000, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Hangzhou Hospital of TCM 453 Ti Yu Chang Road, Hangzhou 310007, China.
authors.forename: Xiao-Long
authors.initials: XL
authors.lastname: He
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002478:Cells, Cultured; D019610:Cytoprotection; D019040:E-Selectin / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D011794:Quercetin / Q000031:analogs & derivatives* / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D019040:E-Selectin; C573420:ICAM1 protein, human; D016328:NF-kappa B; C546936:SELE protein, human; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; C047368:3-methylquercetin; D018799:Intercellular Adhesion Molecule-1; D011794:Quercetin; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III
keywords: AP-1; E-selectin; HUVECs; ICAM-1; Isorhamnetin; NF-κB; VCAM-1; apoptosis; eNOS