上海第二医科大学学报(英文版)
上海第二醫科大學學報(英文版)
상해제이의과대학학보(영문판)
JOURNAL OF SHANGHAI SECOND MEDICAL UNIVERSITY
2000年
1期
64-66,70
,共4页
朱洪生%王胜%沈莉%谢芳%魏丕敬
硃洪生%王勝%瀋莉%謝芳%魏丕敬
주홍생%왕성%침리%사방%위비경
heat shock%SOD%ROS%anoxia- reoxygenation
Objective To explore the role of reaction oxygen species (ROS) in heat shock (HS) on the tolerance of cardiomyocytes to anoxia - reoxygenation (AO - RO) injury and on the activity of superoxide dismutase (SOD).Methods Cultured neonatal myocytes of rats were divided into 5 groups: normal control, anoxic control, HS,HS- SOD pretreated and exogenous ROS pretreated (n= 6). Results Compared with the 2 control groups, ROS release in HS and ROS pretreated groups increased mildly, but after experiencing 3h anoxia/lh reoxygenation 24hlater, ROS release of the two groups decreased significantly, which was accompanied by enhanced SOD activities and less myocytes damage. Opposite results were found when SOD was insituted during HS. Conclusion HS did enhance myocardial tolerance to AO-RO injury. The mild release of ROS during HS may trigger delayed myocardial protection by altering SOD activity.
