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机构地区:[1]第三军医大学新桥医院麻醉科,重庆400037
出 处:《重庆医学》2003年第8期963-964,共2页Chongqing medicine
摘 要:目的 研究自由基在心肌细胞缺氧性DNA损伤和凋亡中的作用。方法 将培养的大鼠心肌细胞随机分成 5组 ,即对照组、缺氧 2 4h组、SOD组、CAT组和SOD +CAT组。然后除对照组外 ,分别加入SOD、CAT或SOD +CAT的各用药组和缺氧2 4h组均缺氧培养 2 4h(其中SOD和CAT的浓度均为 4 0 0 μg/ml) ,终止培养后分别用单细胞微量凝胶电泳检测心肌细胞DNA的损伤和TUNEL标记检测细胞凋亡。结果 缺氧 2 4h后 ,各组心肌细胞核DNA明显受损 ,细胞发生凋亡。与单纯缺氧 2 4h组相比 ,SOD组、CAT组和SOD +CAT组的DNA损伤程度明显减轻 ,受损的细胞数明显减少 (P <0 .0 5 ) ,其中SOD +CAT组更显著(P <0 .0 1 ) ,细胞凋亡的数量也明显减少 (P <0 .0 5 )。结论 自由基参与了心肌细胞缺氧过程中细胞核DNA的断裂损伤和细胞凋亡 ,使用自由基清除剂能减轻其缺氧损伤 。Objective To investigate the roles of free radicals in DNA damages and apoptosis in cardiomyocytes during prolonged hypoxia.Methods Cultured neonatal rat cardiomyocytes were randomly assigned to control group, hypoxia for 24h group, SOD group, CAT group and SOD+CAT group. Then SOD or CAT or SOD and CAT were added into in the last three groups respectively, and the final concentrations of SOD or CAT was 400μg per milliliter.Apart from those in control group, cardiomyocytes in other groups were cultured under hypoxia for 24h.The DNA damages were detected with single cell gel electrophoresis and apoptosis cells were measured by TUNEL label in individual cardiomyocyte after the culture was ended. Results In comparison with the control group, the DNA strands were damaged significantly and apoptosis was induced remarkably after hypoxia for 24h ( P <0.01) in other groups, but the degree of DNA damage was less serious and the number of DNA damaged cells or apoptosis cells was significantly fewer in SOD group, CAT group and especially in SOD + CAT group than in hypoxia for 24h group( P <0.05).Conclusion Free radicals participate in DNA damages and apoptosis of cultured cardiomyocytes during hypoxia, and the use of radical scavengers might protect cardiomyocytes from DNA damages and apoptosis induced by hypoxia.
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