| TTX通过JAK2/STAT3通路活化SOD减轻心肌细胞凋亡 |
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| 引用本文： | 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(1) |
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| 作者姓名： | 刘胜中 杨双强 |
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| 作者单位： | 四川省医学科学院·四川省人民医院胸心外科,成都,610072;重庆医科大学附属第一医院胸心外科,重庆,400016 |
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| 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30rain后,灌注4℃ TTX心脏停搏液,停搏心脏并低温维持60 min,复灌K-H缓冲液60 min后,取左心室肌备用.TTX+AG490组:操作同℃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(Apoptosis index,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.
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| 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 |
Tetrodotoxin cardiaoplegia decreases cardiomyocytes apoptosis through JAK2/STAT3 pathway inducing the activation of SOD |
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| 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, 2010, 35(1) |
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| Authors: | LIU Sheng-zhong et al |
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| Affiliation: | LIU Sheng-zhong,et al(Department of Cardiothoracic Surgery,Sichuan Academy of Medical Sciences & Sichuan People's Hospital) |
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| 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... |
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