title: Protection of endothelial cells against Ang II-induced impairment: Involvement of both PPARα and PPARγ via PI3K/Akt pathway.
abstract: The aim of our study is to explore the involvement of PPARα and PPARγ in Ang II-induced endothelial injury. We found that Ang II significantly elevated the oxidative stress in HUVECs, causing apoptosis and cellular impairment in a time-dependent pattern. Activation of either PPARα by docosahexaenoic acid (DHA) or PPARγ by rosiglitazone protected the endothelial cells. Interestingly, a more significant effect was observed when DHA and rosiglitazone were administrated together. Moreover, we found that this protection was mediated through the PI3K/Akt pathway. Our study may help to understand the mechanism of endothelial dysfunction, contributing to the treatment of hypertension and other endothelial-related diseases.
authors.affiliation: a Department of General Practice , The First Affiliated Hospital of China Medical University , Shenyang , China.
authors.forename: HaiYan
authors.initials: H
authors.lastname: Shan
authors.affiliation: b Science Experiment Center , China Medical University , Shenyang , China.
authors.forename: Siyang
authors.initials: S
authors.lastname: Zhang
authors.affiliation: a Department of General Practice , The First Affiliated Hospital of China Medical University , Shenyang , China.
authors.forename: Xiaojie
authors.initials: X
authors.lastname: Wei
authors.affiliation: c Department of Epidemiology , College of Public Health China Medical University , Shenyang , China.
authors.forename: Xuelian
authors.initials: X
authors.lastname: Li
authors.affiliation: a Department of General Practice , The First Affiliated Hospital of China Medical University , Shenyang , China.
authors.forename: Huimeng
authors.initials: H
authors.lastname: Qi
authors.affiliation: a Department of General Practice , The First Affiliated Hospital of China Medical University , Shenyang , China.
authors.forename: Yini
authors.initials: Y
authors.lastname: He
authors.affiliation: a Department of General Practice , The First Affiliated Hospital of China Medical University , Shenyang , China.
authors.forename: Ao
authors.initials: A
authors.lastname: Liu
authors.affiliation: a Department of General Practice , The First Affiliated Hospital of China Medical University , Shenyang , China.
authors.forename: Donghui
authors.initials: D
authors.lastname: Luo
authors.affiliation: a Department of General Practice , The First Affiliated Hospital of China Medical University , Shenyang , China.
authors.forename: Xiaosong
authors.initials: X
authors.lastname: Yu
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D017209:Apoptosis / Q000187:drug effects; D002478:Cells, Cultured; D019610:Cytoprotection / Q000502:physiology; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D042783:Endothelial Cells / Q000187:drug effects / Q000502:physiology; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D006973:Hypertension; D018384:Oxidative Stress / Q000187:drug effects*; D047493:PPAR alpha / Q000378:metabolism*; D047495:PPAR gamma / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D000077154:Rosiglitazone; D015398:Signal Transduction / Q000187:drug effects; D045162:Thiazolidinediones / Q000494:pharmacology*
chemical_list: D047493:PPAR alpha; D047495:PPAR gamma; D020011:Protective Agents; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D000804:Angiotensin II; D004281:Docosahexaenoic Acids; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt
keywords: Angiotensin II; PI3K/Akt pathway; PPARα; PPARγ; endothelial dysfunction