a Department of General Practice , The First Affiliated Hospital of China Medical University , Shenyang , China.
b Science Experiment Center , China Medical University , Shenyang , China.
Clin Exp Hypertens. 2016;38(7):571-577. doi: 10.3109/10641963.2016.1174248. Epub 2016 Sep 20.
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.
本研究旨在探讨过氧化物酶体增殖物激活受体α（PPARα）和过氧化物酶体增殖物激活受体γ（PPARγ）在血管紧张素Ⅱ（AngⅡ）诱导的内皮损伤中的作用。我们发现 AngⅡ可显著增加人脐静脉内皮细胞（HUVEC）的氧化应激，引起细胞凋亡和功能障碍，呈时间依赖性。二十二碳六烯酸（DHA）激活 PPARα或罗格列酮激活 PPARγ均可对内皮细胞起保护作用，当 DHA 和罗格列酮同时给药时，可观察到更显著的效果。此外，我们发现这种保护作用是通过 PI3K/Akt 通路介导的。本研究可能有助于理解内皮功能障碍的机制，为高血压和其他与内皮相关的疾病的治疗提供帮助。
