Journal
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
Volume 31, Issue 6, Pages 1381-1387Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2013.1334
Keywords
advanced glycation end product; apoptosis; endothelial cell; hydrogen; reactive oxygen species
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Funding
- National Natural Science Foundation of China [30872710, 30770852]
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The purpose of the present study was to determine whether using hydrogen-rich medium (FIRM) to increase hydrogen levels in endothelial cells (ECs) protects ECs from apoptosis induced by advanced glycation end products (AGEs). The thoracic aorta was removed from 2-3-year-old Sprague-Dawley rats, and ECs were isolated and cultured. After culturing ECs in the presence of AGEs and/or with HRM for 24 h, Annexin V/7-AAD and TUNEL staining were carried out to detect apoptosis. Intracellular ROS were detected by fluorescent probe and quantified by flow cytometry. The expression of antioxidative enzymes (superoxide dismutase, glutathione peroxidase) was determined by real-time PCR analysis and enzymatic assay. The relative expression levels of Bcl-2 and Bax were analyzed by western blotting. The addition of AGEs increased the apoptosis of ECs in a concentration-dependent manner and FIRM reduced the AGE (400 mu g/ml)-induced apoptosis from 21.61 +/- 2.52 to 11.32 +/- 1.75%. HRM also significantly attenuated the AGE-induced intracellular ROS induction and decrease in the expression of antioxidative enzymes. In conclusion, hydrogen exhibits significant protective effects against AGE-induced EC injury possibly through reducing ROS generation, intracellular antioxidant enzyme system protection and elevation of the Bcl-2/Bax ratio.
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