摘要
目的:了解活性氧自由基对心肌细胞的损伤状况,并在此基础上探讨非促分裂型haFGF(nm -haFGF)对心肌细胞的保护作用。方法:采用胰蛋白酶消化法,体外分离和培养新生SD乳鼠心肌细胞,建立H2 O2 损伤心肌细胞的模型,检测细胞存活率、细胞凋亡和观察细胞形态学的变化,以评价H2 O2 对心肌细胞的损伤状况,并加入一定浓度的nm -haFGF ,观察心肌细胞的存活率、SOD活性和MDA含量的改变,以及凋亡的变化。结果:H2 O2对心肌细胞的损伤呈浓度依赖地加剧;在H2 O2 压力作用下,10 - 80 μg/Lnm -haFGF逐步提高H2 O2 损伤心肌细胞的存活率,其中80 μg/L组的细胞存活力明显大于对照组(P <0 . 0 5 ) ,同时逐步提高SOD活性和降低MDA含量,其中4 0和80 μg/L组的SOD活性明显大于阳性对照组(P <0 .0 5 ) ,4 0和80 μg/L组的MDA含量明显小于阳性对照组(P <0. 0 5 ) ;此外,在0. 0 1mmol/LH2 O2 作用2 4h后,10 μg/L和4 0 μg/Lnm -haFGF组的心肌细胞凋亡百分率分别为32 . 4 %和10 . 7%。结论:心肌细胞的损伤与H2 O2 的浓度呈剂量依赖关系;nm -haFGF对由H2 O2 引起的心肌细胞损伤具有拮抗作用。
AIM: To study the protective effects of n on -mitogenic human fibroblast growth factor (nm-haFGF) on cardiomyocytes injured b y reactive oxygen free radicals. METHODS: The cardiomyocytes were isolated from neonatal SD mouse by trypsin digestion. The cardiomyocytes injury model was established by expos ing the cells to hydrogen peroxide (H 2O 2), and the injury status in cardiomy ocytes were evaluated by examining the cellular viability, measuring cell apopto sis and observing the change of cellular morphology. nm-haFGF was added to the c ulture medium, and the changes of cellular viability, superoxide dismutase (SOD) , malondialdehyde (MDA) and celluar apoptosis were observed. RESULTS: A dose-dependence relation between the concentration of H 2O 2 and the cardiomyocytes injury was observed. 10-80 μg/L nm-haFGF dose -dependently increased cardiomyocyte viability and the general SOD activity, as well as decreased the content of MDA and the quantity of cardiomyocyte apoptosis . CONCLUSION: The higher the concentration of H 2O 2, the mor e serious the cardiomyocyte injury. nm-haFGF may have a good protective effects on cardiomyocytes treated with H 2O 2.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第4期679-684,共6页
Chinese Journal of Pathophysiology
基金
国家 8 6 3计划项目 (No .2 0 0 1AA2 15 131)
国家"十五"创新药物重大专项资助项目 (No .2 0 0 2AA2Z3318)
关键词
成纤维细胞生长因子
过氧化氢
心肌
Fibroblast growth factors
Hydrogen peroxide
Myocardium
