Apelin attenuated hydrogen peroxide-induced cell death in endothelial cells by decreasing the intracellular ROS levels.

Abstract

Apelin plays an important role in the proliferation of vascular endothelial cells, and the expression of apelin is enhanced after ischemic stroke. Since the production of reactive oxygen species (ROS) including hydrogen peroxide (H₂O₂) is elevated in the post-ischemic brain, the proliferated endothelial cells are subjected to oxidative stress. However, the effects of apelin on oxidative stress-induced injury in endothelial cells are poorly investigated. In this study we investigated the effect of apelin on H₂O₂-induced cell death in mouse endothelial cell line bEnd.3. Cell viability was determined by a colorimetric 3,4,5-dimethylthiazol-2-yl-2,5-diphenyl tetrazolium bromide (MTT) assay, and intracellular ROS levels were evaluated by dihydroethidium (DHE) staining. Treatment of bEnd.3 cells with H₂O₂ (150 µM) increased DHE-positive cells and induced cell death. Pretreatment with [Pyr1]-apelin-13 (10 µM) for 24 h reduced the increase in the number of DHE-positive cells and attenuated the cell death. These results suggest that apelin protects bEnd.3 cells from H₂O₂-induced cell death by decreasing the intracellular ROS levels.