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. 2019 Jan 12;20(2):294. doi: 10.3390/ijms20020294

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Conclusion of the current study. The current study demonstrates that ritonavir (RTV), an HAART drug, can cause oxidative stress and endothelial dysfunction by increase of ROS production and decrease of expression of SOD1, SOD2 and eNOS in human endothelial cells. Thus, RTV-induced oxidative stress and endothelial dysfunction could contribute to cardiovascular disease. On the other hand, ginsenoside Rb1 can effectively block the effects of RTV via a unique mechanism by which Rb1 specifically binds to and activates ER-β and induces upregulation of SOD1, SOD2 and eNOS in human endothelial cells. Rb1 can also directly scavenge ROS.