摘要
目的探讨粒细胞集落刺激因子(G-CSF)对急性心肌梗死(AMI)大鼠血清及心肌组织中一氧化氮(NO)、丙二醛(MDA)和超氧化物歧化酶(SOD)含量的影响.方法通过结扎冠状动脉前降支建立急性心肌梗死(AMI)大鼠模型,将AMI大鼠随机分为G-CSF治疗组(GAMI组)、心肌梗死对照组(AMI组)和假手术组(SO组),GAMI组模型制备后3h给予生理盐水稀释的rhG-CSF(浓度为2mg/L)皮下注射10μg/kg/d,共5d.AMI组和SO组3h后给予等量的生理盐水皮下注射,共5d.最后一次给药后24h取各组大鼠血清及心肌组织检测NO、MDA、SOD的含量.结果 AMI组大鼠血清和心肌组织中MDA水平显著高于SO组(P<0.01),NO、SOD值显著低于SO组(P<0.01).GAMI组大鼠血清和心肌组织中MDA水平显著低于AMI组(P<0.05),NO、SOD值显著高于AMI组(P<0.05).结论 G-CSF能提高NO含量,增强SOD的活性.降低MDA的含量,对急性心肌梗死具有明显的保护作用.
Objective To investigate the influence of granulocyte colony stimulating factor (G-CSF) on nitric oxide (NO). malondialdehyde (MDA) and superoxide dismutase (SOD) content in serum and cardiac tissue of acute myocardial infarction (AMI) rats. Methods The rat models of myocardial infarction established by ligation of anterior descending coronary artery were divided randomly into 3 groups including G-CSF treatment group (GAMI group), myocardial infarction control group (AMI group) and sham operation group (SO group), and rhG-csF was injected, which was diluted with normal saline (concentration of 2 rag/L) 10 μg/kg/d after the GAMI group model had completed 3 hours for 5 days. Rats of AMI and SO group were injected the same amount of saline 3 hours later for 5 days. NO. MDA. SOD contents in serum and myocardial tissue of every group were tested 24 hours after the last administration. Results Compared with that of SO group, MDA in the serum and cardiac muscle of acute myocardial infarction increased significantly ( P 〈0.01), NO and SOD content decreased significantly ( P 〈0.01) in AMI group. In comparison with that of AMI group, MDA decreased significantly ( P 〈0.05), NO and SOD increased significantly in G-CSF group ( P 〈0, 05). Conclusion G-CSF can increase the content of NO, activity of SOD, and reduce the content of MDA in acute myocardial infarction rats. The mechanism of protecting acute myocardial infarction may has relationship with the effect that it transfers bone marrow stem cell to the damaged heart and further d3fferentiate to cardiac muscle cell and endothelial cell, thus participating oxygen-free-radical clearing activity and anti-lipid peroxidation.
出处
《河北北方学院学报(自然科学版)》
2011年第6期86-89,共4页
Journal of Hebei North University:Natural Science Edition
基金
河北省中医药管理局项目(编号:2009146)