精胺抑制模拟缺血-再灌注心肌细胞Fas/FasL的表达

目的：观察外源性精胺对缺血-再灌注损伤诱导的乳鼠心肌细胞凋亡的影响并探讨其可能机制。方法：原代培养的乳鼠心肌细胞缺氧、无血清孵育2h，再复氧和复血清培养24h以模拟心肌缺血-再灌注损伤，并于再灌注期给予10μmol/L的外源性精胺。利用流式细胞仪检测心肌细胞的凋亡率；电镜观察细胞超微结构变化；应用RT-PCR、Westernblotting方法和免疫荧光的方法观察Fas、FasLmRNA的转录和蛋白的表达。结果：模拟缺血-再灌注后心肌细胞凋亡率为27.4%±1.8%，明显高于对照组（5.7%±0.3%），细胞超微结构出现凋亡、坏死等改变，Fas、FasL的转录和蛋白表达均明显上调，与对照组比，FasmRNA和FasLmRNA转录分别增加了2.2倍和2.4倍（P<0.01）；Fas和FasL的蛋白表达分别增加了1.7倍和1.9倍（P<0.01）；10μmol/L的外源性精胺干预后心肌细胞凋亡率降低为21.7%±1.3%，Fas、FasL的转录和蛋白表达也明显被抑制（与单纯模拟缺血-再灌注组比，P<0.05或P<0.01）。结论：外源性精胺可通过抑制Fas死亡受体途径而减轻模拟缺血-再灌注诱导的心肌细胞凋亡。

Spermine inhibits expression of Fas/FasL in simulated ischemia-reperfusion-injured cardiomyocytes of neonatal rat

AIM:To explore the effects and possible mechanism of exogenous spermine on the apoptosis of primary cultured neonatal cardiomyocytes induced by simulated ischemia-reperfusion (I/R) injury. METHODS: To establish a model of simulated I/R,the primary cultured neonatal rat cardiomyocytes were incubated in ischemia-mimetic solution (under the conditions of hypoxia plus serum deprivation) for 2 h,and re-incubated the cells in normal culture medium for 24 h. The apoptotic cell death was assayed by flow cytometry. ...