Application of Ginsenoside-Rg1 Could Not Ameliorate The Hyperoxic-Induced Vascular Endothelial Oxidative Stress and Apoptosis
Abstract Background: Oxygen therapy is necessary to preterm infants with respiratory distress. However, hyperoxia may cause bronchopulmonary dysplasia and retinopathy of prematurity due to suppression of vasogenesis and increase of cell death. Ginsenoside-Rg1, one of the active components of Ginsen, is shown as a proangiogenic factor of vascular endothelial cells. We evaluated whether application of Ginsenoside-Rg1 is able to improve hyperoxic-induced vascular endothelium injury.Materials and methods: Human umbilical vein endothelial cells (HUVECs) were cultured under room air and 60% oxygen for 72 hours, respectively. Gensenoside-Rg1 was added to the medium at 0, 75, 150, 300nM. HUVECs proliferation, oxidative stress and apoptosis under normoxic and hyperoxic conditions were assayed by Western Blot.Results: Under hyperoxia (60% O2), HUVECs proliferation and levels of vascular endothelial growth factor (VEGF) were significantly decreased after ginsenoside-Rg1 treatment. Interestingly, both levels of glucocorticoid receptor (GR) and glutathione peroxidase (GPx) were increased after 72 hr Ginsenoside-Rg1 treatment, but no changed under room air control. The levels of oxidative stress-induced Bax and cytochrome c and apoptosis-related active caspase 3 and poly ADP-ribose polymerase were significantly increased after ginsenoside-Rg1 treatment under hyperoxic condition.Discussion and conclusion: In HUVECs model, Ginsenoside-Rg1 is unable to overcome the major hyperoxic-induced vascular endothelium injury. It might aggravate oxidative stress and endothelial apoptosis caused by oxygen toxicity. However, both elevated levels of GR and GPx indicate that Ginsenoside-Rg1 could be involved in vascular signaling and the regulation of oxidative stress under hyperoxia. Further investigation of Rg1 effects under hyperoxia is required.