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.

KEYWORDS:

• Angiotensin II
• endothelial dysfunction
• PI3K/Akt pathway
• PPARα
• PPARγ

Acknowledgments

We thank Dr. Ying Chang (Institut Pasteur de Lille, France) for critical review of the manuscript, we are also grateful to Dr. Lei Yang (China Medical University) for valuable technical contributions.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

Funding

The study was supported by grants from the National Natural Science Foundation of China (No.81200245), the specialized researcher fund for the doctoral program of Higher Education (No.20122104120003), the Science and Technology Project of Liaoning Province (No.2012225091, 201202263), and Major Basic Project of China (No.2013CB530804).

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Funding

The study was supported by grants from the National Natural Science Foundation of China (No.81200245), the specialized researcher fund for the doctoral program of Higher Education (No.20122104120003), the Science and Technology Project of Liaoning Province (No.2012225091, 201202263), and Major Basic Project of China (No.2013CB530804).