内源性神经激肽和降钙素基因相关肽在大鼠心肌缺血后适应对心肌超氧化物歧化酶的作用 |
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引用本文: | 贾晓鹰,郭政,郭建丽,刘亚兵.内源性神经激肽和降钙素基因相关肽在大鼠心肌缺血后适应对心肌超氧化物歧化酶的作用[J].现代保健,2013(10):8-9. |
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作者姓名: | 贾晓鹰 郭政 郭建丽 刘亚兵 |
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作者单位: | [1]山西医科大学,山西太原030001 [2]山西医科大学第二医院,山西太原030001 |
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基金项目: | 国家自然科学基金(编号:30972860) |
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摘 要: | 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(350~400g)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30min,再灌注120min)、ipost组(结扎冠状动脉左前降支30min,再灌注10s夹闭10s,如此反复3次后持续再灌注120min)、CGRP8-37+ipost组(结扎冠状动脉左前降支25min,按1μg/kg剂量从尾静脉给药CGRP8-37,5min行后处理再灌注同ipost组)、D-SP+ipost组(结扎冠状动脉左前降支25min,按1μg/kg剂量从尾静脉给药D-SP,5min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。
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关 键 词: | NK1受体 CGRP受体 缺血后适应 超氧化物歧化酶 Caspase-3 |
The Role of Endogenous Neurokinin and CGRP to Myocardial Superoxide Dismutase of Ischemic Postconditioning in Rats |
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Institution: | JIA Xiaoying, GUO Zheng, GUO Jian-li, (Medical Innovation of China, 2013, 10 ( 10 ) : 008-009) |
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Abstract: | 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 ( 1 μg/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 ( 1 μg/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. |
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Keywords: | NK1 receptor CGRP receptor Ischemic postconditioning SOD Caspase-3 |
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