摘要
目的 :研究能量治疗对心力衰竭的治疗机制。观察磷酸肌酸 (phosphocreatine,CP)对心肌细胞线粒体膜电位的保护作用。方法 :采用胶原酶分离成年大鼠心肌细胞 ,0 .2 mmol/ L H2 O2 刺激细胞 ,于刺激前 10 min加入 10mm ol/ L CP,利用荧光探针 JC-1结合流式细胞仪检测线粒体膜电位的变化 ;Annexin-V/ PI及 TUNEL 染色法鉴定心肌细胞的凋亡。结果 :H2 O2 导致线粒体膜电位下降 ,细胞凋亡增加。CP有效地减低了线粒体膜电位的下降 ,减少了细胞凋亡。结论 :CP能够抗心肌细胞氧化损伤 ,其机制可能依赖于减少或抑制线粒体膜电位的下降 。
AIM: To observe the protective effect of phosph ocreatine on mitochondrial function in rat cardiomyocytes.METHODS: Using H 2O 2 to cause ox idative stress, CP was given ten minutes before H 2O 2 stimulation. JC-1 in combi nation with flow cytometry was used to measure the changes of mitochondrial me mbrane potential. Apoptosis was identified by means of double fluorescence st aining with Annexin V-FITC/propidim iodide and TUNEL staining. RESULTS : H 2O 2 caused the decrease of mitochondrial membrane potential and the increase of apoptosis rate. But in the CP treatment group, mitochondrial membrane potential wasn't decreased significantly. CONCLUSION: CP can prevent the cardio myocyte fr om oxidative injury. The mechanism may rely on inhibiting the decrease of mitoc hondrial membrane potential and protecting mitochondrial function.
出处
《心脏杂志》
CAS
2004年第1期14-16,共3页
Chinese Heart Journal
关键词
线粒体膜电位
磷酸肌酸
细胞凋亡
mitochondrial membrane potential
phosphocreatine
apoptosis
