Abstract: Objective To elucidate the influence of soluble form of receptor for advanced glycation end products (sRAGE) on hypoxia/reoxygenation myocardial oxidative stress. Methods Cardiac myocytes were isolated from neonatal rats with the modified 2-step collagenase digest method and were subjected to Primary culture for 48 hours. Hypoxia 3 h/reoxygenation 2 h injury model was produced. The cells were randomly divided into four groups: normoxic control group (Con), normoxia + sRAGE group(Con-sRAGE), hypoxia/reoxygenation (H/R) group(model group), hypoxia/reoxygenation + sRAGE (H/R-sRAGE) group (experimental group). The viability of myocardial cells was detected by MTT; The leakage of lactate dehydrogenase in culture medium (LDH); the activity of superoxide dismutase (SOD) were detected by xanthine oxidase; The content of malondialdehyde (MDA) was detected by thiobarbituric acid color method; The intensity of fluorescence was detected by DCFH-DA fluorescent probe combined flow cytometry-Reactive oxygen species (ROS) levels in response; nitrate reductase determination of nitric oxide (NO) levels. Results Compared with H/R group, H/R-sRAGE group could improve the myocardial viability, reduce the amount of LDH leakage, increase SOD activity, lower MDA and ROS levels (P<0.05). Conclusion sRAGE may act directly on myocardial cells and antagonize the hypoxia/reoxygenation injury, the protective role is related to inhibition of oxidative stress.

Key words: soluble form of receptor for advanced glycation end products, myocardial cells, hypoxia/reoxygenation, oxidative stress