海南医学
海南醫學
해남의학
HAINAN MEDICAL JOURNAL
2014年
21期
3124-3126
,共3页
心肌缺血再灌注损伤%脑利钠肽%凋亡%氧化应激
心肌缺血再灌註損傷%腦利鈉肽%凋亡%氧化應激
심기결혈재관주손상%뇌리납태%조망%양화응격
Myocardial ischemia-reperfusion injury%Brain natriuretic peptide (BNP)%Apoptosis%Oxidative stress
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)、BNP0.005组及BNP0.01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(Apoptoticindex，AI)。结果S组、I/R组、BNP0.005组、BNP0.01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BNP0.005组，BNP0.01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。
目的：探討腦利鈉肽對心肌缺血再灌註損傷心肌細胞凋亡的保護作用。方法將24隻SD雄性大鼠隨機分入對照組(S組)、缺血/再灌註組(I/R組)、BNP0.005組及BNP0.01組，每組6隻，製作在體心肌缺血再灌註模型，分彆使用上述榦預，再灌註結束後摘取心髒，檢測心肌標本超氧化物歧化酶(Superoxidedismutase，SOD)、丙二醛(Malondiadehyde，MDA)及心肌細胞凋亡指數(Apoptoticindex，AI)。結果S組、I/R組、BNP0.005組、BNP0.01組SOD分彆為(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分彆為(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分彆為(3.84±2.53)%/(43.63±3.70)%/(22.13±2.85)%、(14.21±2.77)%。各組間SOD、MDA活力及AI差異均具有統計學意義(P<0.001)；相較于其他組，BNP各組均具有較高的SOD活力和更低的MDA活力及AI水平(P<0.001)，而相較于BNP0.005組，BNP0.01組SOD活力更高(P=0.001)，MDA活力及AI水平更低(P值分彆為0.007和0.012)。結論BNP後處理可能通過減少氧自由基而對缺血再灌註損傷的心肌具有保護作用，且這種保護作用可能與濃度相關。
목적：탐토뇌리납태대심기결혈재관주손상심기세포조망적보호작용。방법장24지SD웅성대서수궤분입대조조(S조)、결혈/재관주조(I/R조)、BNP0.005조급BNP0.01조，매조6지，제작재체심기결혈재관주모형，분별사용상술간예，재관주결속후적취심장，검측심기표본초양화물기화매(Superoxidedismutase，SOD)、병이철(Malondiadehyde，MDA)급심기세포조망지수(Apoptoticindex，AI)。결과S조、I/R조、BNP0.005조、BNP0.01조SOD분별위(195.78±21.45)U/mg、(84.35±9.03)U/mg、(125.66±18.06)U/mg、(161.83±15.49)U/mg；MDA분별위(2.73±0.41)nmol/mg、(7.36±0.51)nmol/mg、(4.46±0.47)nmol/mg、(3.69±0.38)nmol/mg；AI분별위(3.84±2.53)%/(43.63±3.70)%/(22.13±2.85)%、(14.21±2.77)%。각조간SOD、MDA활력급AI차이균구유통계학의의(P<0.001)；상교우기타조，BNP각조균구유교고적SOD활력화경저적MDA활력급AI수평(P<0.001)，이상교우BNP0.005조，BNP0.01조SOD활력경고(P=0.001)，MDA활력급AI수평경저(P치분별위0.007화0.012)。결론BNP후처리가능통과감소양자유기이대결혈재관주손상적심기구유보호작용，차저충보호작용가능여농도상관。
Objective To evaluate the effects of brain natriuretic peptide (BNP) postconditioning on myocar-dial 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 min);BNP 0.005 group (n=6, 0.005μg/(kg·min) BNP injected to caudal vein by syringe pump for 10 min after ischemia surgery);BNP 0.01 group (n=6, 0.005μg/(kg·min) BNP injected to caudal vein by syringe pump for 10 min af-ter 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, BNP 0.005 group and BNP 0.01 group, SOD levels were (195.78±21.45) U/mg, (84.35±9.03) U/mg, (125.66±18.06) U/mg, (161.83±15.49) U/mg, re-spectively;MDA levels were (2.73±0.41) nmol/mg, (7.36±0.51) nmol/mg, (4.46±0.47) nmol/mg, (3.69±0.38) nmol/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 significant-ly 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.
