中文摘要：

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;（2）I/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、Beclin1（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：

Objective： To investigate the role of Notch1 pathway and its underlying mechanisms in adult mice subjected to is- chemia/reperfusion （l/R） injury induced by high temperature and humidity. Methods： Adult C57 mice were divided into six groups：①Sham group; ②FR group; ③high temperature and humidity group; ④high temperature and humidity ＋I/R group; ⑤high temperature and humidity＋Jaggedl （an activator of Notchl）＋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 ofNotchl intracellular domain （Notchl ICD）, Hairy and enhancer of split （Hesl）, microtubule-associated proteinl light chain 3 （LC3）, Beclinl and p62 were analyzed by Western blot. Results： Compared with the sham group, I/R injury significantly reduced the cardiac function, increased the myocardial infarct size, and increased the expression ofNotchl ICD, Hesl, LC3- II / I and Beclin 1 （except p62）. Although high temperature and humidity also reduced the cardiac Rmction and increased the myocardial infarct size, it reduced the expression ofNotchl ICD, Hesl, LC3- II / I and Beclinl （except p62） compared with sham group. In addition, com- pared with UR group or high temperature and humidity group, high temperature and humidity ＋I/R group fia＇ther reduced the cardiac function, increased the myocardial infarct size, and decreased the expression ofNotchl ICD, Hesl, LC3- II / I and Beclinl （except p62）. Moreover, compared with high temperature and humidity ＋I/R group, adding Jaggedl （an activator of Notchl） improved the cardiac function, reduced the myocardial infarct size, and increased the expression ofNotchl ICD, Hesl, LC3- II / I and Beclinl （except p62）. Conclusions： Activation of Notchl pathway might alleviate the myocardial ischemia/reperfusion injury induced by high temperature and humidity t