Tetrodotoxin cardiaoplegia decreases cardiomyocytes apoptosis through JAK2/STAT3 pathway inducing the activation of SOD

LIU Sheng-zhong; et al

doi:10.13406/j.cnki.cyxb.2010.01.012

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Tetrodotoxin cardiaoplegia decreases cardiomyocytes apoptosis through JAK2/STAT3 pathway inducing the activation of SOD

更新时间：2024-01-17

- Tetrodotoxin cardiaoplegia decreases cardiomyocytes apoptosis through JAK2/STAT3 pathway inducing the activation of SOD
- Journal of Chongqing Medical University Vol. 35, Issue 1, Pages: 64-67(2010)
- 作者机构：
  
  1. 四川省医学科学院·四川省人民医院胸心外科
  2. 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.2010.01.012
  CLC： R541
- Published：2010，
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[1]刘胜中,杨双强.TTX通过JAK2/STAT3通路活化SOD减轻心肌细胞凋亡[J].重庆医科大学学报,2010,35(01):64-67.

LIU Sheng-zhong, et al. Tetrodotoxin cardiaoplegia decreases cardiomyocytes apoptosis through JAK2/STAT3 pathway inducing the activation of SOD. [J]. Journal of Chongqing Medical University 35(1):64-67(2010)
[1]刘胜中,杨双强.TTX通过JAK2/STAT3通路活化SOD减轻心肌细胞凋亡[J].重庆医科大学学报,2010,35(01):64-67. DOI： 10.13406/j.cnki.cyxb.2010.01.012.

LIU Sheng-zhong, et al. Tetrodotoxin cardiaoplegia decreases cardiomyocytes apoptosis through JAK2/STAT3 pathway inducing the activation of SOD. [J]. Journal of Chongqing Medical University 35(1):64-67(2010) DOI： 10.13406/j.cnki.cyxb.2010.01.012.

摘要

目的:研究JAK2/STAT3信号通路在河豚毒素（Tetrodotoxin

TTX）心脏停搏液心肌保护中的作用。方法:24只Wistar大鼠随机均分为对照组、TTX组和TTX+AG490组

每组8只。对照组:开胸取左心室肌作为缺血前对照。TTX组:建立离体心脏Langendorff-Neely灌注模型

预灌注K-H缓冲液30min后

灌注4℃TTX心脏停搏液

停搏心脏并低温维持60min

复灌K-H缓冲液60min后

取左心室肌备用。TTX+AG490组:操作同TTX组

但预灌和复灌时均在K-H缓冲液中加入JAK2抑制剂AG490（5μmol/L）。分别采用免疫组化法、比色法和TUNEL法测定心肌组织中p-STAT3、SOD活性和MDA含量

以及心肌细胞凋亡指数（Apoptosisindex

AI）

并比较组间的变化。结果:与对照组相比

TTX组和TTX+AG490组p-STAT3表达量均明显增加（P<0.05）;予以AG490处理后

p-STAT3表达量较TTX组明显下降（P<0.05）。与对照组相比

TTX组和TTX+AG490组SOD活性和MDA含量均明显增加（P<0.05）;予以AG490处理后

SOD活性较TTX组显著降低（P<0.05）

MDA含量却明显增加（P<0.05）。经历缺血再灌注后

TTX组和TTX+AG490组心肌细胞AI明显高于对照组（P<0.05）;与TTX组相比

TTX+AG490组AI显著增加（P<0.05）。结论:JAK2/STAT3信号通路通过增强SOD活性

减轻膜脂质过氧化损伤

减少心肌细胞凋亡

介导TTX心脏停搏液对缺血心肌的保护作用。

Abstract

Objective:To investigate the effect of JAK2/STAT3 pathway on myocardial protection of tetrodotoxin(TTX) cardioplegia in rat hearts.Methods:24 wistar rats were randomly divided into group control

group TTX and group TTX+AG490(n=8).The left ventricular samples in group control were collected as pre-ischemia control through thoracotomy.After isolated heart langendorff and neely models were established the rat hearts in group TTX were continuously perfused with krebs-henseleit(K-H)buffer solution for 30 minutes

arrested by TTX cardioplegia(4℃)for 60 minutes

underwent reperfusion with K-H buffer solution for 60 minutes

and then the left ventricular samples were collected for detection.The rat hearts in group TTX+AG490 were perfused and reperfused with JAK2 inhibitor AG490(5 μmol/L) and K-H buffer solution under the same procedure as group TTX.The protein expression indexes(PEI) of phosphorylated-STAT3(p-STAT3)in myocardium were detected by immunohistochemical assay(IHC).Both the activity of superoxide dismutase(SOD)and the content of maleic dialdehyde(MDA)in myocardial tissue homogenate were detected by colorimetry.The apoptosis index(AI)of cardiomyocyte was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL).The changes of these indexes in three groups were used for comparison.Results:Compared with group control

the PEI of p-STAT3 in group TTX and group TTX+AG490 increased significantly(P<0.05).Treated with AG490

the PEI of p-STAT3 in group TTX+AG490 was lower than that in group TTX(P<0.05).Compared with group control

the activity of SOD and the content of MDA in Group TTX and group TTX+AG490 increased significantly(P<0.05).Treated with AG490

the activity of SOD in group TTX+AG490 was lower than that in group TTX(P<0.05)

but the content of MDA was higher than that in group TTX(P<0.05).After ischemia/reperfusion

AI in group TTX and group TTX+AG490 was significantly higher than that in group control(P<0.05);compared with group TTX

AI in group TTX+AG490 increased significantly(P<0.05).Conclusions:JAK2/STAT3 pathway could mediate myocardial protection of TTX cardioplegia in rat hearts via inducing the activity of SOD to alleviate membrane lipid peroxidation injury and decreasing cardiomyocytes apoptosis.

关键词

信号转导及转录激活因子3超氧化物歧化酶凋亡河豚毒素心肌保护

Keywords

Signal transducer andactivator of transcription3superoxide dismutaseapoptosisTetrodotoxinmyocardial protection

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