Protective effects of prostaglandin E1 on human umbilical vein endothelial cell injury induced by hydrogen peroxide
Abstract
Aim: To investigate the protective effects of prostaglandin E1 (PGE1) 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 μmol/L) for 24 h and exposed to H2O2 (200 μmol/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: PGE1 (0.25−1.00 μmol/L) was able to markedly restore the viability of HUVECs under oxidative stress, and scavenged intracellular reactive oxygen species induced by H2O2. PGE1 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, PGE1 significantly increased NO content, eNOS protein, and mRNA expression.
Conclusion: PGE1 effectively protected endothelial cells against oxidative stress induced by H2O2, an activity that might depend on the up-regulation of NO expression.
Keywords:
Methods: HUVECs were pretreated with PGE1 (0.25, 0.50, and 1.00 μmol/L) for 24 h and exposed to H2O2 (200 μmol/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: PGE1 (0.25−1.00 μmol/L) was able to markedly restore the viability of HUVECs under oxidative stress, and scavenged intracellular reactive oxygen species induced by H2O2. PGE1 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, PGE1 significantly increased NO content, eNOS protein, and mRNA expression.
Conclusion: PGE1 effectively protected endothelial cells against oxidative stress induced by H2O2, an activity that might depend on the up-regulation of NO expression.