摘要
背景：氢已被证明对心肌发挥生物活性作用。该研究检查了氢减弱缺血 - 再灌注损伤的信号传导途径。 方法：20只雄性Wistar大鼠共检测富氢水对心脏缺血再灌注的影响。采用左心室组织进行蛋白质芯片技术筛选和分析活性蛋白因子。通过使用基因本体论（GO）富集原理获得KEGG途径的富集。 Western blot和免疫组化检测JAK2，STAT1，STAT3，p-STAT1，p-JAK2，p-STAT3在大鼠心肌中的表达。通过TUNEL染色检测对照和富氢水组的凋亡率。 结果：富含氢的水组中25种蛋白质（包括5种转导途径）的表达水平下调。与对照组相比，富含氢的水组中p-JAK2 / JAK2，p-STAT3 / STAT3的表达水平上调，并且与对照组相比，富含氢的水组中p-STAT1 / STAT1下调。 。此外，富氢水组的凋亡率也显着降低。 结论：富氢水可通过上调JAK2-STAT3信号通路的表达抑制缺血再灌注损伤后心肌细胞的凋亡，从而减少缺血再灌注损伤。
关键词: 富氢水，缺血再灌注损伤，JAK-STAT信号通路，蛋白芯片技术，细胞凋亡。
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