Protective effects of celastrol against γ irradiation-induced oxidative stress in human umbilical vein endothelial cells

• Published in: Experimental and therapeutic medicine Vol. 16; no. 2; pp. 685 - 694
• Main Authors: Han, Xiang-Bei, Tan, Yan, Fang, Yan-Qiu, Li, Feng
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications UK Ltd 01.08.2018; D.A. Spandidos
• Subjects: Antioxidants; Apoptosis; Cell culture; Cytotoxicity; Deoxyribonucleic acid; DNA; Enzymes; Free radicals; Lipid peroxidation; Lipids; Nitric oxide; Oxidative stress; Protein expression; Proteins; Rodents; Studies; Variance analysis; Beijing China; United States > US; China; celastrol; antioxidant enzymes; human umbilical vein endothelial cells; reactive oxygen species; γ irradiation
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2018.6270

High-dose ionizing radiation can cause harmful effects on the cardiovascular system. Notably, endothelial cells are critical targets in radiation-induced damage. γ radiation exerts its biological effects through the radiolysis of water, which further generates ROS and induces lipid peroxidation and DNA damage. The present study aimed to evaluate the potential protective effects of celastrol against γ radiation-induced oxidative stress in human umbilical vein endothelial cells (HUVECs). HUVECs were exposed to γ radiation at different doses with or without celastrol treatment. Cell viability and cytotoxicity, migratory ability, ROS production, lipid peroxidation, oxidative DNA damage and antioxidative enzyme levels were evaluated in HUVECs at 24 h post-irradiation. It was observed that HUVECs exhibited decreased cell viability, increased cytotoxicity and a decreased migratory ability after exposure to 20-Gy γ radiation. Celastrol treatment concentration-dependently reversed these effects. γ irradiation was also demonstrated to increase the production of ROS, enhance lipid peroxidation and oxidative DNA damage and decrease the levels of SOD, catalase, GST and GPx in HUVECs. These detrimental effects were blocked by treatment with celastrol for 24 h. These data suggested that celastrol not only attenuated γ radiation-induced cytotoxicity, but also effectively blocked oxidative stress in HUVECs. As an antioxidant agent, celastrol may have potential protective effects in HUVECs against γ irradiation-induced injury.