BNP对在体大鼠I/R损伤心肌细胞凋亡及氧化应激的影响  

Effect of BNP on myocardium apoptosis and oxidative stress induced by ischemia/reperfusion injury in rat

作　　者：董小莉[1] 谭宁[2] 邓宇珺[2] 

机构地区：[1]海南省人民医院心血管内科,海南海口570311 [2]广东省医学科学院广东省人民医院广东省心血管病研究所心血管内科,广东广州510080

出　　处：《海南医学》2014年第21期3124-3126,共3页Hainan Medical Journal

基　　金：广东省自然科学基金资助项目(编号:200813030301166;9121008002000002)

摘　　要：目的探讨脑利钠肽对心肌缺血再灌注损伤心肌细胞凋亡的保护作用。方法将24只SD雄性大鼠随机分入对照组(S组)、缺血/再灌注组(I/R组)、BNP 0.005组及BNP 0.01组,每组6只,制作在体心肌缺血再灌注模型,分别使用上述干预,再灌注结束后摘取心脏,检测心肌标本超氧化物歧化酶(Superoxidedismutase,SOD)、丙二醛(Malondiadehyde,MDA)及心肌细胞凋亡指数(Apoptotic index,AI)。结果 S组、I/R组、BNP 0.005组、BNP 0.01组SOD分别为(195.78±21.45)U/mg、(84.35±9.03)U/mg、(125.66±18.06)U/mg、(161.83±15.49)U/mg;MDA分别为(2.73±0.41)nmol/mg、(7.36±0.51)nmol/mg、(4.46±0.47)nmol/mg、(3.69±0.38)nmol/mg;AI分别为(3.84±2.53)%/(43.63±3.70)%/(22.13±2.85)%、(14.21±2.77)%。各组间SOD、MDA活力及AI差异均具有统计学意义(P<0.001);相较于其他组,BNP各组均具有较高的SOD活力和更低的MDA活力及AI水平(P<0.001),而相较于BNP 0.005组,BNP 0.01组SOD活力更高(P=0.001),MDA活力及AI水平更低(P值分别为0.007和0.012)。结论 BNP后处理可能通过减少氧自由基而对缺血再灌注损伤的心肌具有保护作用,且这种保护作用可能与浓度相关。Objective To evaluate the effects of brain natriuretic peptide （BNP） postconditioning on myocardial apoptosis during myocardial ischemia/reperfusion injury in a rat model. Methods Twenty four male Sprague Dawley rats were randomized into four groups： sham operation group （S group, n=6, the breast tissue was dissected without ligation of left anterior descending branch）; ischemic/reperfusion group （I/R group, n=6, ischemia/reperfusion surgery by ligation of left anterior descending branch, followed by saline injected to caudal vein through syringe pump for 10 rain）; BNT 0.005 group （n=6, 0.005 μg/（kg.min） BNP injected to caudal vein by syringe pump for 10 min after ischemia surgery）; BNP 0.01 group （n=6, 0.005 μg/（kg, rain） BNP injected to caudal vein by syringe pump for 10 min after ischemia surgery）. At the end of reperfusion, heart was harvested, and myocardium superoxide dismutase （SOD）, Malo- ndiadehyde （MDA） and Apoptotic index （AI） were detected. Results In S group, I/R group, BNT 0.005 group and BNT 0.01 group, SOD levels were （195.78±21.45） U/rag, （84.35±9.03） U/mg, （125.66±18.06） U/mg, （161.83±15.49） U/mg, respectively; MDA levels were （2.73±0.41） nmol/mg, （7.36±0.51） umol/mg, （4.46±0.47） nmol/mg, （3.69±0.38） umol/mg, respectively; AI were （3.84± 2.53）%, （43.63±3.70）%, （22.13±2.85）%, （14.21±2.77）%, respectively. The differences between the groups were all statistically significant （P〈0.001）. BNP 0.005 group and BNP 0.01 group had significantly higher SOD activity, lower MDA activity and lower AI level than other groups （P〈0.001）. Compared with BNP 0.005 group, BNP 0.01 group had significantly higher SOD activity （P=-0.001）, lower MDA activity （P=-0.007） and lower AI level （P=0.012）. Conclusion BNP postconditioning could reduce the oxygen free radicals level to protect the ischemia-reperfusion myocardial injury. This effect is positively correlated with BNP levels.

关 键 词：心肌缺血再灌注损伤 脑利钠肽 凋亡 氧化应激 

分 类 号：R-332[医药卫生]