| 吕 平,李 巍,杨亚丽,吴 萌,胡建华,纪兆乐,尹志勇,李 妍.激活Notch1通过促进自噬改善高温高湿条件下心肌缺血/再灌注损伤[J].,2017,17(9):1623-1627 |
| 激活Notch1通过促进自噬改善高温高湿条件下心肌缺血/再灌注损伤 |
| Activation of Notch1 Pathway Alleviated Myocardial Ischemia/reperfusion Injury induced by High Temperature and Humidity through Promoting Autophagy |
| 投稿时间：2016-10-10 修订日期：2016-10-30 |
| DOI：10.13241/j.cnki.pmb.2017.09.006 |
| 中文关键词: Notch1 自噬 缺血/再灌注损伤 高温高湿 |
| 英文关键词: Notch1 Autophagy Ischemia/reperfusion injury High temperature and humidity |
| 基金项目:全军后勤科研面上项目（CWS14J065）；国家自然科学基金面上项目（81570252;81500195） |
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| 中文摘要: |
| 摘要 目的：明确Notch1通路在高温高湿条件下小鼠心肌缺血/再灌注(ischemia/reperfusion, I/R)损伤中的作用及其潜在机制。方法：将成年C57小鼠随机分为①假手术组；②I/R组；③高温高湿组；④高温高湿+I/R组；⑤高温高湿+Jagged1(Notch1激动剂)+I/R组；⑥高温高湿+溶剂+I/R组。采用超声心动图检测心功能，伊文氏蓝/2,3,5-三苯基氯化四氮唑双染法检测心肌梗死面积，Western blot检测Notch1细胞内段(Notch1 intracellular domain, Notch1 ICD)、Hairy和分裂增强子(Hairy and enhancer of split，Hes1)、微管相关蛋白1轻链3(microtubule-associated protein1 light chain 3，LC3)、Beclin1和p62的蛋白表达水平。结果：与假手术组对比，I/R组心功能下降，心肌梗死面积增加，Notch1 ICD、Hes1、LC3-Ⅱ/Ⅰ、Beclin1(p62相应降低)表达升高，而高温高湿组心功能下降，心肌梗死面积增加，Notch1 ICD、Hes1、LC3-Ⅱ/Ⅰ、Beclin1(p62相应升高)表达降低；和I/R组或高温高湿组对比，高温高湿+I/R组心功能进一步下降，心肌梗死面积进一步增加，Notch1 ICD、Hes1、LC3-Ⅱ/Ⅰ、Beclin1(p62进一步升高)表达进一步降低；和高温高湿+I/R组对比，加入Notch1激动剂Jagged1后，心功能提高，心肌梗死面积缩小，Notch1 ICD、Hes1、LC3-Ⅱ/Ⅰ、Be- clin1(p62相应降低)表达升高。结论：激活Notch1通路可能通过促进自噬从而缓解高温高湿所致的心肌缺血/再灌注损伤。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the role of Notch1 pathway and its underlying mechanisms in adult mice subjected to is- chemia/reperfusion (I/R) injury induced by high temperature and humidity. Methods: Adult C57 mice were divided into six groups:①Sham group; ②I/R group; ③high temperature and humidity group; ④high temperature and humidity +I/R group; ⑤high temperature and humidity+Jagged1(an activator of Notch1)+I/R group; ⑥high temperature and humidity+ Vehicle +I/R group. The cardiac function was determined by echocardiography and myocardial infarct size was evaluated by Evans Blue/2,3,5-triphenyltetrazolium chloride (TTC) staining. The expressions of Notch1 intracellular domain (Notch1 ICD), Hairy and enhancer of split (Hes1), microtubule-associated pro- tein1 light chain 3 (LC3), Beclin1 and p62 were analyzed by Western blot. Results: Compared with the sham group, I/R injury signifi- cantly reduced the cardiac function, increased the myocardial infarct size, and increased the expression of Notch1 ICD, Hes1, LC3-Ⅱ/Ⅰand Beclin1(except p62). Although high temperature and humidity also reduced the cardiac function and increased the myocardial infarct size, it reduced the expression of Notch1 ICD, Hes1, LC3-Ⅱ/Ⅰand Beclin1(except p62) compared with sham group. In addition, com- pared with I/R group or high temperature and humidity group, high temperature and humidity +I/R group further reduced the cardiac function, increased the myocardial infarct size, and decreased the expression of Notch1 ICD, Hes1, LC3-Ⅱ/Ⅰand Beclin1(except p62). Moreover, compared with high temperature and humidity +I/R group, adding Jagged1 (an activator of Notch1) improved the cardiac function, reduced the myocardial infarct size, and increased the expression of Notch1 ICD, Hes1, LC3-Ⅱ/Ⅰand Beclin1(except p62). Conclusion: Activation of Notch1 pathway might alleviate the myocardial ischemia/reperfusion injury induced by high temperature and humidity through promoting autophagy. |
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