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首页> 外文期刊>Scandinavian journal of clinical and laboratory investigation. >The heme oxygenase inducer hemin protects against cardiac dysfunction and ventricular fibrillation in ischaemic/reperfused rat hearts: role of connexin 43.
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The heme oxygenase inducer hemin protects against cardiac dysfunction and ventricular fibrillation in ischaemic/reperfused rat hearts: role of connexin 43.

机译:血红素加氧酶诱导剂血红素可预防缺血/再灌注大鼠心脏的心脏功能障碍和心室纤颤:连接蛋白43的作用。

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摘要

Cardiac expression of cytoprotective gene heme oxygenase-1 (HO-1) is modulated by ischaemia and reperfusion (I/R). We therefore hypothesized that pretreatment with hemin, an inductor of HO-1, would precondition the heart against post-ischaemic dysfunction and ventricular fibrillation (VF). Male Wistar rats were given either hemin or HO enzyme inhibitor zinc protoporphyrin IX (ZnPP IX). Isolated hearts were subjected to 30 min global ischaemia followed by 120 min of reperfusion or were aerobically perfused in a time-matched non-ischaemic protocol. Control animals received no pretreatment. Compared to non-perfused controls, pretreatment with hemin increased HO-1 mRNA 13-fold (p<0.001) and HO-1 protein 3.5-fold (p
机译:缺血和再灌注(I / R)调节细胞保护基因血红素加氧酶-1(HO-1)的心脏表达。因此,我们假设用血红素(HO-1的诱导剂)进行预处理将使心脏免于缺血后功能障碍和心室纤颤(VF)。给雄性Wistar大鼠给予血红素或HO酶抑制剂锌原卟啉IX(ZnPP IX)。离体心脏经历了30分钟的整体缺血,然后进行了120分钟的再灌注,或者以时间匹配的非局部缺血方案进行了有氧灌注。对照动物未接受预处理。与未灌注的对照相比,用血红素预处理可增加HO-1 mRNA的13倍(p <0.001)和HO-1蛋白3.5倍(p

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