Protective effects of prostaglandin E1 on human umbilical vein endothelial cell injury induced by hydrogen peroxide

被引:29
作者
Fang, Wen-tong [2 ]
Li, Hong-jian [1 ]
Zhou, Liao-sheng [3 ]
机构
[1] Qianfoshan Hosp Shandong Prov, Dept Pharm, Jinan 250014, Peoples R China
[2] Shandong Univ, Dept Clin Pharm, Sch Pharm, Jinan 250012, Peoples R China
[3] Qianfoshan Hosp Shandong Prov, Dept Geriatr Med, Jinan 250014, Peoples R China
关键词
prostaglandin E-1; human umbilical vein endothelial cells; hydrogen peroxide; apoptosis; nitric oxide; NITRIC-OXIDE; RESPONSIVE ELEMENT; ENOS EXPRESSION; IN-VIVO; GROWTH; GENE; ANGIOGENESIS; TOXICITY; SURVIVAL; ICARIIN;
D O I
10.1038/aps.2010.23
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
Aim: To investigate the protective effects of prostaglandin E-1 (PGE(1)) against H2O2-induced oxidative damage on human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were pretreated with PGE1 ( 0.25, 0.50, and 1.00 mu mol/L) for 24 h and exposed to H2O2 ( 200 mu mol/L) for 12 h, and cell viability was measured by the MTT assay. LDH, NO, SOD, GSH-Px, MDA, ROS, and apoptotic percentage were determined. eNOS expression was measured by Western blotting and real-time PCR. Results: PGE(1) (0.25-1.00 mu mol/L) was able to markedly restore the viability of HUVECs under oxidative stress, and scavenged intracellular reactive oxygen species induced by H2O2. PG(E)1 also suppressed the production of lipid peroxides, such as MDA, restored the activities of endogenous antioxidants including SOD and GSH-Px, and inhibited cell apoptosis. In addition, PGE(1) significantly increased NO content, eNOS protein, and mRNA expression. Conclusion: PGE(1) effectively protected endothelial cells against oxidative stress induced by H2O2, an activity that might depend on the up-regulation of NO expression.
引用
收藏
页码:485 / 492
页数:8
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