Introduction of antioxidant-loaded liposomes into endothelial cell surfaces through DNA hybridization

被引：6

作者：

Deno, Sho ^{[1
]}

Takemoto, Naohiro ^{[1
]}

Iwata, Hiroo ^{[1
]}

机构：

[1] Kyoto Univ, Inst Frontier Med Sci, Dept Reparat Mat, Sakyo Ku, Kyoto 6068507, Japan

来源：

BIOORGANIC & MEDICINAL CHEMISTRY | 2014年 / 22卷 / 01期

关键词：

Ischemia; Reperfusion injury; Endothelial cell; Surface modification; Vitamin E; Liposome; Poly(ethylene glycol)-phospholipid; DNA hybridization; PANCREATIC-ISLETS; INTRAPORTAL TRANSPLANTATION; REPERFUSION INJURY; ALPHA-TOCOPHEROL; FLOW-CYTOMETRY; HUMAN BLOOD; ACTIVATION; LANGERHANS; ISCHEMIA; DAMAGE;

D O I：

10.1016/j.bmc.2013.11.023

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Ischemia-reperfusion damage is a problem in organ transplantation. Reactive oxygen species are produced in cells by blood-mediated reactions at the time of blood reperfusion. In this study, we developed a method to immobilize and internalize antioxidants in endothelial cells, using vitamin E-loaded liposomes. The liposomes loaded with vitamin E and human umbilical vein endothelial cells (HUVECs) were modified with poly(ethylene glycol)-phospholipid conjugates carrying 20-mer of deoxyadenylic acid (oligo(dA)(20)) and 20-mer of complementary deoxythymidylic acid (oligo(dT)(20)), respectively. The liposomes were effectively immobilized on HUVECs through DNA hybridization between oligo(dA)(20) and oligo(dT)(20). The liposomes loaded with vitamin E were gradually internalized into HUVECs. Then, the cells were treated with antimycin A to induce oxidative stress. We found the amount of reactive oxygen species was greatly reduced in HUVECs carrying vitamin E-loaded liposomes. (C) 2013 Elsevier Ltd. All rights reserved.

引用

页码：350 / 357

页数：8

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