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. 2017 Feb 9;18(2):77. doi: 10.3390/ijms18020077

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© 2017 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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The molecular mechanism of the GP-17 anti-atherosclerotic effects. ROS induced by Ox-LDL result in endotheliocyte apoptosis and oxidative stress. GP-17 activates the ERα-mediated PI3K/Akt pathway, further resulting in Nrf2/HO-1 up-regulation and increasing the level of antioxidant enzymes. This process attenuates Ox-LDL-induced oxidative injury. Furthermore. GP-17 inhibited Ox-LDL-mediated HUVEC apoptosis by decreasing the ratio of Bax to Bcl-2 and controlling cleaved caspase-3 activation. This process inhibits Ox-LDL-induced endothelial cell apoptosis via the ERα-mediated PI3K/Akt pathway. T bars represented inhibition and arrows represented activation.