摘要
目的 研究缺氧在新生大鼠心肌细胞凋亡中的作用及一氧化氮 (NO)的保护作用。方法 取体外培养的新生大鼠心肌细胞置 95 0mL/LN2 ,5 0mL/LCO2 孵箱中培养16 ,32和 48h ,造成缺氧损伤的细胞模型 ,观察凋亡发生的情况 ;将NO供体SNAP加入培养基中 ,使其终浓度为 10 0μmol/L ,置于上述缺氧环境中培养 16 ,32和 48h ,检测细胞凋亡。结果在缺氧条件下培养 16 ,32 ,48h后 ,心肌细胞的凋亡率分别为 :( 2 9± 0 5 ) % ,( 6 2± 0 8) %和 ( 2 6 6±3 0 ) % ;而加入NO供体后 ,凋亡率分别为 :( 0 2± 0 3) % ,( 3 4± 0 4) %和 ( 11 8± 1 2 ) %。结论凋亡是心肌细胞缺氧损伤的主要形式 ;
Aim To study the role of hypoxiainduced apoptosis in neonatal rat cardiomyocyte and the protection effect of nitric oxide(NO). Methods Neonatal rat cardiomyocytes were cultured in an incubator of 950 mL/L N 2 and 50 mL/L CO 2 for 16, 32 and 48 h to create cell models of hypoxia injury and detect apoptosis. And NO donor SNAP at 100 μ mol/L was added to the models. Apoptosis was detected in the hypoxia cells without or with No treatment. Results After hypoxia of 16, 32 and 48 h,the apoptosis rates of cardiomyocytes were 29% ± 05% , 62% ± 08% and 266% ± 30% , respectively. Whereas the apoptosis rates of cells treated with SNAP were 02% ± 03% , 34% ± 04% and 118% ± 12% , respectively. Conclusion Apoptosis is the main form of hypoxia injury in cardiomyocytes; NO protect cardiomyocytes from apoptosis induced by hypoxia.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
2000年第3期225-227,共3页
Chinese Journal of Cellular and Molecular Immunology
