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首页|期刊导航|中国药理学通报|Hedgehog通路对心肌梗死及心肌细胞缺血缺氧的作用机制研究

Hedgehog通路对心肌梗死及心肌细胞缺血缺氧的作用机制研究

陈瑶 余细勇

中国药理学通报2016,Vol.32Issue(5):676-680,681,6.
中国药理学通报2016,Vol.32Issue(5):676-680,681,6.DOI:10.3969/j.issn.1001-1978.2016.05.016

Hedgehog通路对心肌梗死及心肌细胞缺血缺氧的作用机制研究

Effect of Hedgehog pathway on myocardial infarction and hypoxic-ischemic cardiomyocytes

陈瑶 1余细勇1

作者信息

  • 1. 广东省心血管病研究所、广东省人民医院,广东 广州 510080
  • 折叠

摘要

Abstract

Aim To investigate the effect of Sonic Hedgehog on normal hearts and hypoxic-ischemic myo-cardial cells. Methods A method for left anterior de-scending artery ( LAD ) ligation was employed to con-struct the myocardial infarction model, and ultrasonic cardiogram was used for identification. Western blot and immunofluorescence staining were used to detect expressions of Shh, Ptch-1, Smo and Gli-1 in H9C2 cells and H2 O2-induced H9C2 cells, and that in 12 ca-ses of myocardial infarction tissues and 9 cases of nor-mal myocardium, respectively. Agonist and antagonist of Shh pathway were adminstered in the hypoxic-ische-mic myocardial H2 O2-induced H9C2 cell model, and once again expressions and strength of Shh, Ptch-1, Smo, Gli-1 were detected. Results Shh and Gli-1 were not expressed in normal hearts, but expressed in hearts with myocardial infarction;Ptch-1 and Smo were expressed in both normal hearts and hearts with myo-cardial infarction. Under the action of agonist, expres-sions of Shh and Gli-1 increased in the hypoxic-ische-mic H9C2 cell model. Similarly, Shh and Gli-1 were not expressed in normal H9C2 cells, but in H2 O2-in-duced H9C2 cells, and Ptch-1 and Smo were expressed in both normal H9C2 and in H2 O2-induced H9C2 cells. Conclusion Shh signaling pathway can be acti-vated in the condition of ischemia and oxidative stress, and then it promotes the repairing of myocardial cell damage.

关键词

Hedgehog 通路/心肌梗死/缺血/缺氧/H2 O2/心肌细胞

Key words

Hedgehog pathway/myocardial infarc-tion/ischemia/hypoxia/H2 O2/myocardial cells

分类

医药卫生

引用本文复制引用

陈瑶,余细勇..Hedgehog通路对心肌梗死及心肌细胞缺血缺氧的作用机制研究[J].中国药理学通报,2016,32(5):676-680,681,6.

基金项目

国家自然科学基金资助项目( No 81120108003,81330007) ( No 81120108003,81330007)

广东省科技计划重点项目(No 2014 A050503047,2015B020225006) (No 2014 A050503047,2015B020225006)

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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