Urocortin-postconditioning protects heart from ischemia-reperfusion injury through interfering mitochondria-dependent apoptotic pathway

OU Yuan; et al

doi:10.13406/j.cnki.cyxb.2010.08.004

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Urocortin-postconditioning protects heart from ischemia-reperfusion injury through interfering mitochondria-dependent apoptotic pathway

更新时间：2024-01-17

- Urocortin-postconditioning protects heart from ischemia-reperfusion injury through interfering mitochondria-dependent apoptotic pathway
- Journal of Chongqing Medical University Vol. 35, Issue 8, Pages: 1187-1190(2010)
- 作者机构：
  
  重庆医科大学附属第一医院胸心外科
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2010.08.004
  CLC： R363
- Published：2010，
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[1]欧袁,杨双强,辛东.Urocortin后处理抑制线粒体凋亡通路保护心肌缺血再灌注损伤[J].重庆医科大学学报,2010,35(08):1187-1190.

OU Yuan, et al. Urocortin-postconditioning protects heart from ischemia-reperfusion injury through interfering mitochondria-dependent apoptotic pathway. [J]. Journal of Chongqing Medical University 35(8):1187-1190(2010)
[1]欧袁,杨双强,辛东.Urocortin后处理抑制线粒体凋亡通路保护心肌缺血再灌注损伤[J].重庆医科大学学报,2010,35(08):1187-1190. DOI： 10.13406/j.cnki.cyxb.2010.08.004.

OU Yuan, et al. Urocortin-postconditioning protects heart from ischemia-reperfusion injury through interfering mitochondria-dependent apoptotic pathway. [J]. Journal of Chongqing Medical University 35(8):1187-1190(2010) DOI： 10.13406/j.cnki.cyxb.2010.08.004.

摘要

目的:研究Urocortin（UCN）后处理对缺血大鼠心肌线粒体凋亡通路的影响

探讨其心肌保护的可能机制。方法:24只Wistar大鼠随机分为3组

每组8只

分为对照组（CON）

缺血再灌注组（I/R）

Urocortin（UCN）组。CON组大鼠麻醉后直接开胸取左心室肌作缺血前对照。I/R组

建立离体心脏Langendorff-Neely模型

灌注K-H缓冲液30min后

主动脉根部灌注4℃St.Thomas-2心脏停搏液

低温下心脏停跳30min

复灌K-H缓冲液90min后

取左心室肌备检。UCN组

低温下心脏停跳30min后

复灌含Urocortin浓度为10-8mol/L的K-H缓冲液90min

取左心室肌备检。蛋白免疫印迹（Western blot）法检测各组心肌细胞线粒体凋亡通路的标志性蛋白CytoC从线粒体的释放

免疫组化法检测各组心肌细胞Caspase-3蛋白的表达。原位末端转移酶标记法（TUNEL）检测心肌细胞凋亡。结果:Western blot检测显示CON组

I/R组

UCN组胞浆中CytoC量分别为0.56±0.05

1.29±0.02

0.88±0.07

I/R组

UCN组高于CON组（P<0.05）

UCN组低于I/R组（P<0.05）;免疫组化显示CON组

I/R组

UCN组Caspase-3蛋白表达量分别为0.15±0.22

0.36±0.15

0.24±0.20

I/R组

UCN组高于CON组（P<0.05）

UCN组低于I/R组（P<0.05）;各组心肌细胞凋亡指数分别为2.29±0.67

12.81±0.62

6.77±1.12

I/R组

UCN组高于CON组（P<0.05）

UCN组低于I/R组（P<0.05）。Caspase-3蛋白表达与胞浆中CytoC含量呈正相关（r=0.775

P<0.05）;心肌组织中心肌细胞凋亡指数与胞浆中CytoC含量呈正相关（r=0.865

P<0.05）。结论:Urocortin后处理能够抑制细胞凋亡

其机制可能与抑制线粒体释放CytoC和随后的Caspase-3的激活

抑制线粒体通路的细胞凋亡有关。

Abstract

Objective:To investigate the effects of Urocortin-postconditioning on mitochondria-dependentapoptotic pathway.Methods: 24 Wistar rats were randomly divided into 3 groups(n=8):Control group(CON)

I/R group(I/R)

Urocortin group(UCN).The left ventricular samples in the Control group were collected as pre-ischemia controls through thoracotomy.After isolated heart Langendoff and Neely models were established

the rat hearts in the I/R group and the UCN group were continuously perfused with Krebs-Henseleit (K-H)buffersolution for 30 min

then the rat hearts were arrested by cardioplegia

St.Thomas-2 solution(STH-2)for 30min.After that

the rat hearts in the I/R group were reperfused with K-H buffer solution for 90 min.The rat hearts in the UCN group were reperfused with K-H buffer solution containing 10-8 mol/L Urocortin for 90 min.The releasing of Cyto C protein into cytosol was detected by Western blot.The expression of Caspase-3 protein in cardiomyocyte was detected by immunohistochemical assay.The apoptosis index (AI)of cardiomyocyte was detected by TUNEL.Results:Compared with Control group

the expression ofCaspase-3 and Cyto Cprotein in the I/R group and the UCN group were significantly increased(P<0.05).Caspase-3 and Cyto C protein in the UCN group were lowly expressed than those in the I/R group(0.24±0.70 vs 0.36±0.15

P<0.05

0.88±0.07 vs 1.29±0.02

P<0.05).After reperfusion

apoptosis index(AI)in the I/R group and UCN group were significantly higher than that in the Control group(P<0.05);Compared with I/R group group

AI in UCN group was decreased increased(6.77±1.12 vs 12.81±0.62

P<0.05).The expression of Caspase-3 protein had a positive correlation with Cyto C protein in cytosol(r=0.775

P<0.05)

and the apoptosis index(AI)of cardiomyocyte had a positive correlation with Cyto Cprotein in cytosol(r=0.865

P<0.05)。Conclusion:Urocortin protect hearts from ischemic-reperfusion injury through interfering mitochondria-dependent apoptotic pathway.

关键词

Urocortin心肌保护细胞凋亡半光氨酸基天冬氨酸特异性蛋白酶-3细胞色素C

Keywords

Urocortinmyocardial protectionapoptosisCaspase-3CytoC

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