中国医学创新
中國醫學創新
중국의학창신
MEDICAL INNOVATION OF CHINA
2013年
10期
8-9
,共2页
贾晓鹰%郭政%郭建丽%刘亚兵
賈曉鷹%郭政%郭建麗%劉亞兵
가효응%곽정%곽건려%류아병
NK1受体%CGRP受体%缺血后适应%超氧化物歧化酶%Caspase-3
NK1受體%CGRP受體%缺血後適應%超氧化物歧化酶%Caspase-3
NK1수체%CGRP수체%결혈후괄응%초양화물기화매%Caspase-3
NK1 receptor%CGRP receptor%Ischemic postconditioning%SOD%Caspase-3
目的:研究神经激肽1(NK1)、降钙素基因相关肽(CGRP)在大鼠缺血后适应对心肌超氧化物歧化酶(SOD)的作用.方法:随机将SD雄性大鼠(350~400 g)分为5组:sham组(只穿线不结扎冠状动脉)、I/R组(结扎冠状动脉左前降支30 min,再灌注120 min)、ipost组(结扎冠状动脉左前降支30 min,再灌注10 s夹闭10 s,如此反复3次后持续再灌注120 min)、CGRP8-37+ipost组(结扎冠状动脉左前降支25 min,按1μg/kg剂量从尾静脉给药CGRP8-37,5 min行后处理再灌注同ipost组)、D-SP+ipost组(结扎冠状动脉左前降支25 min,按1μg/kg剂量从尾静脉给药D-SP,5 min行后处理再灌注同ipost组);快速液氮冷冻各组缺血心肌组织并提取心肌总蛋白,行总蛋白定量,用酶联免疫吸附技术检测心肌SOD的表达,分光光度法检测Caspase-3活性.结果:(1)与sham组比较,I/R组Caspase-3、SOD均增多(P<0.01);(2)与I/R组比较,ipost组SOD增多(P>0.05),Caspase-3减少(P<0.01);(3)与ipost组比较:CGRP8-37+ipost组SOD降低(P<0.01),Caspase-3增多(P>0.05),D-SP+ipost组SOD降低(P<0.01),Caspase-3增多(P>0.05).结论:神经激肽1降钙素基因相关肽(CGRP)通过上调缺血心肌SOD表达对缺血后适应心肌起保护作用.
目的:研究神經激肽1(NK1)、降鈣素基因相關肽(CGRP)在大鼠缺血後適應對心肌超氧化物歧化酶(SOD)的作用.方法:隨機將SD雄性大鼠(350~400 g)分為5組:sham組(隻穿線不結扎冠狀動脈)、I/R組(結扎冠狀動脈左前降支30 min,再灌註120 min)、ipost組(結扎冠狀動脈左前降支30 min,再灌註10 s夾閉10 s,如此反複3次後持續再灌註120 min)、CGRP8-37+ipost組(結扎冠狀動脈左前降支25 min,按1μg/kg劑量從尾靜脈給藥CGRP8-37,5 min行後處理再灌註同ipost組)、D-SP+ipost組(結扎冠狀動脈左前降支25 min,按1μg/kg劑量從尾靜脈給藥D-SP,5 min行後處理再灌註同ipost組);快速液氮冷凍各組缺血心肌組織併提取心肌總蛋白,行總蛋白定量,用酶聯免疫吸附技術檢測心肌SOD的錶達,分光光度法檢測Caspase-3活性.結果:(1)與sham組比較,I/R組Caspase-3、SOD均增多(P<0.01);(2)與I/R組比較,ipost組SOD增多(P>0.05),Caspase-3減少(P<0.01);(3)與ipost組比較:CGRP8-37+ipost組SOD降低(P<0.01),Caspase-3增多(P>0.05),D-SP+ipost組SOD降低(P<0.01),Caspase-3增多(P>0.05).結論:神經激肽1降鈣素基因相關肽(CGRP)通過上調缺血心肌SOD錶達對缺血後適應心肌起保護作用.
목적:연구신경격태1(NK1)、강개소기인상관태(CGRP)재대서결혈후괄응대심기초양화물기화매(SOD)적작용.방법:수궤장SD웅성대서(350~400 g)분위5조:sham조(지천선불결찰관상동맥)、I/R조(결찰관상동맥좌전강지30 min,재관주120 min)、ipost조(결찰관상동맥좌전강지30 min,재관주10 s협폐10 s,여차반복3차후지속재관주120 min)、CGRP8-37+ipost조(결찰관상동맥좌전강지25 min,안1μg/kg제량종미정맥급약CGRP8-37,5 min행후처리재관주동ipost조)、D-SP+ipost조(결찰관상동맥좌전강지25 min,안1μg/kg제량종미정맥급약D-SP,5 min행후처리재관주동ipost조);쾌속액담냉동각조결혈심기조직병제취심기총단백,행총단백정량,용매련면역흡부기술검측심기SOD적표체,분광광도법검측Caspase-3활성.결과:(1)여sham조비교,I/R조Caspase-3、SOD균증다(P<0.01);(2)여I/R조비교,ipost조SOD증다(P>0.05),Caspase-3감소(P<0.01);(3)여ipost조비교:CGRP8-37+ipost조SOD강저(P<0.01),Caspase-3증다(P>0.05),D-SP+ipost조SOD강저(P<0.01),Caspase-3증다(P>0.05).결론:신경격태1강개소기인상관태(CGRP)통과상조결혈심기SOD표체대결혈후괄응심기기보호작용.
Objective:To investigate the role of endogenous neurokinin and CGRP in modulation of myocardial superoxide dismutase in ischemic postconditioning in rats.Method:Adult male SD rats(weighting 350-400 g)were randomly divided into 5 groups:sham group(only threading without ligation of coronary artery),I/R group(ligation of coronary artery for 30 minutes,then reperfusion for 120 minutes),ipost group(ligation of coronary artery for 30 minutes,then repeated three cycles of release of the coronary artery for 10 seconds and 10 seconds of ligation of coronary artery before reperfusion of the heart for 120 minutes),CGRP8-37+ipost group(CGRP8-37,a selective antagonist of CGRP receptor,was given(1μg/kg,i.v.,) through caudal vein at 5 minutes before the ischemic postconditioning),D-SP+ipost group(D-SP,a selective antagonist of neurokinin-1 receptor was injected(1μg/kg)via caudal vein at 5 minutes before the repeated three times of perfusion.The samples of myocardium was collected and frozen iliquid nitrogen and prepared for quantitative analysis. Detection the expression of SOD used Elisa,detection the expression of Caspase-3 used spectrophotometry. Result:(1)Compared with sham group,The expression of Caspase-3 and SOD in I/R group were increased(P<0.01).(2)Compared with I/R group, The expression of SOD in ipost group was increased(P>0.05),The expression of Caspase-3 in ipost group was decreased(P<0.01).(3)Compared with ipost group,The expression of SOD was decreased(P<0.01)in CGRP8-37+ipost group and D-SP+ipost group.The expresson of Caspase-3 was increased(P>0.05)in CGRP8-37+ipost group,D-SP+ipost group,but the difference did not show statistical significance.Conclusion:The results of this study indicate that endogenous neurokinin and CGRP participate in the anti-apoptosis through up-rewgulation of the expression of myocardial superoxide dismutase in ischemic post-conditioning in rats.
