Mediation of JAK2/STAT3 pathway on myocardial protection of tetrodotoxin cardioplegia in rat hearts via upregulating the protein expression of Bcl-2

LIU Sheng-zhong; et al

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Mediation of JAK2/STAT3 pathway on myocardial protection of tetrodotoxin cardioplegia in rat hearts via upregulating the protein expression of Bcl-2

更新时间：2024-01-17

- Mediation of JAK2/STAT3 pathway on myocardial protection of tetrodotoxin cardioplegia in rat hearts via upregulating the protein expression of Bcl-2
- Journal of Chongqing Medical University Issue 2, Pages: 169-172(2008)
- 作者机构：
  
  1. 重庆医科大学附属第一医院胸心外科
  2. 重庆医科大学附属第一医院胸心外科,重庆,400016
- 作者简介：
- 基金信息：
- DOI：
  CLC： R654.2
- Published：2008，
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[1]刘胜中,綦俊,杨双强.JAK2/STAT3通过上调Bcl-2蛋白介导TTX心肌保护作用[J].重庆医科大学学报,2008(02):169-172.

LIU Sheng-zhong, et al. Mediation of JAK2/STAT3 pathway on myocardial protection of tetrodotoxin cardioplegia in rat hearts via upregulating the protein expression of Bcl-2. [J]. Journal of Chongqing Medical University (2):169-172(2008)
[1]刘胜中,綦俊,杨双强.JAK2/STAT3通过上调Bcl-2蛋白介导TTX心肌保护作用[J].重庆医科大学学报,2008(02):169-172. DOI：

LIU Sheng-zhong, et al. Mediation of JAK2/STAT3 pathway on myocardial protection of tetrodotoxin cardioplegia in rat hearts via upregulating the protein expression of Bcl-2. [J]. Journal of Chongqing Medical University (2):169-172(2008) DOI：

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）。采用免疫组化法测定心肌组织中p-STAT3（磷酸化STAT3）和Bcl-2表达量（Protein expression index

PEI）

TUNEL检测心肌细胞凋亡指数（Apoptosis index

AI）

比较2组间的变化。结果:与对照组相比

TTX组和TTX+AG490组心肌组织中p-STAT3和Bcl-2的表达量均明显增加（P<0.05）;予以AG490处理后

p-STAT3和Bcl-2的表达量较TTX组明显下降（P<0.05）。Bcl-2蛋白表达与p-STAT3蛋白表达呈正相关（r=0.743

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信号通路通过上调Bcl-2的表达

抑制心肌细胞凋亡

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:A total of 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

and underwent reperfusion with K-H buffer solution for 60 minutes

then the left ventricular samples were collected for detections.The rat hearts in Group TTX+AG490 were perfused and reperfused with JAK2 inhibitor AG490(5μmol/L) and K-H buffer solution under the same procedure as Group TTX.The protein expression indexes(PEI) of phosphorylated-STAT3(p-STAT3) and B-cell lymphoma-2(Bcl-2) in myocardium were detected by immunohistochemical assay(IHC).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 and Bcl-2 in Group TTX and Group TTX+AG490 increased significantly(P<0.05);Treated with AG490

the PEI of p-STAT3 and Bcl-2 in Group TTX+AG490 was lower than that in Group TTX(P<0.05).The PEI of Bcl-2 had a positive correlation with the PEI of p-STAT3(r=0.743

P<0.05).After ischemia/reperfusion

AI in Group TTX and Group TTX+AG490 were significantly higher than that in Group Control(P<0.05);compared with Group TTX

AI in Group TTX+AG490 increased significantly(P<0.05).Conclutions:JAK2/STAT3 pathway could mediate myocardial protection of TTX cardioplegia in rat hearts via upregulating the protein expression of Bcl-2 and suppressing cardiomyocytes apoptosis.

关键词

信号转导及转录激活因子3Bcl-2凋亡河豚毒素心肌保护

Keywords

Signal transducer and activator of transcription 3Bcl-2apoptosisTetrodotoxinmyocardial protection

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