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. 2015 Aug 25;10(4):1253–1260. doi: 10.3892/etm.2015.2713

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Copyright: © Yang et al. This is an open access article distributed under the terms of a Creative Commons Attribution License.

This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 4.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

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Figure 6. — Possible protective mechanism of taraxasterol and quercetin against oxidative stress-induced injury. Step 1: H₂O₂ increases the release of TNF-α and IL-6 from HUVECs and upregulates the expression of the adhesive molecule VCAM-1 and the co-stimulatory molecule CD80. Step 2: Pretreatment of the HUVECs with taraxasterol or quercetin inhibits the expression of ICAM-1, VCAM-1 and CD80 on the activated HUVECs. Step 3: A decrease in the expression of CD80 results in the inactivation of T cells. Step 4: A decrease in the expression of ICAM-1 and VCAM-1 results in a reduction of leukocyte rolling. The inactivation of T cells and reduced leukocyte rolling are associated with the progression of atherosclerosis. TNF-α, tumor necrosis factor-α; IL-6, interleukin 6; HUVEC, human umbilical cord endothelial cell; VCAM-1, vascular cell adhesion molecule 1; CD, cluster of differentiation; ICAM-1, intracellular adhesion molecule 1.