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Aspirin Inhibits the Production of Reactive Oxygen Species by Downregulating Nox4 and Inducible Nitric Oxide Synthase in Human Endothelial Cells Exposed to Oxidized Low-density Lipoprotein

Chen, Beidong MD, PhD; Zhao, Jinjing MD, PhD; Zhang, Shan MD; Wu, Wei BS; Qi, Ruomei MD, PhD

Journal of Cardiovascular Pharmacology: May 2012 - Volume 59 - Issue 5 - p 405–412
doi: 10.1097/FJC.0b013e318248acba
Original Article

Abstract: Aspirin has antithrombotic activity and is commonly used to protect patients from cardiovascular disease attacks. The present study investigated whether aspirin reduces reactive oxygen species and proinflammatory proteins in oxidized low-density lipoprotein (ox-LDL)–stimulated human umbilical vein endothelial cells. The results showed that aspirin attenuated reactive oxygen species generation induced by ox-LDL and downregulated Nox4 and inducible nitric oxide synthase expression. Redox-sensitive transcription factor nuclear factor kappa B was inactivated by aspirin, significantly preventing nuclear factor kappa B p65 subunit translocation into the nucleus. The expression of the monocyte/macrophage chemotactic protein 1 also decreased, but endothelial nitric oxide synthase expression increased in aspirin-treated cells. Aspirin ameliorated oxidative stress by downregulating Nox4 and inducible nitric oxide synthase and improved endothelial cell function by increasing endothelial nitric oxide synthase expression. Thus, aspirin may possess protective effects against ox-LDL–induced endothelial cell injury.

Beijing Institute of Geriatrics, Beijing Hospital and Key Laboratory of Geriatrics, Ministry of Health, Beijing, China.

Reprints: Ruomei Qi, MD, PhD, Beijing Institute of Geriatrics, Beijing Hospital, No. 1 Dahualu, Beijing 100730, China (e-mail:

Supported by grants from the National Natural Science Foundation of China (grant no. 30471925, 30572083, and 81070231).

The authors report no funding or conflicts of interest.

Received May 24, 2011

Accepted December 28, 2011

© 2012 Lippincott Williams & Wilkins, Inc.