论文部分内容阅读
心肌缺血再灌注损伤可诱发心肌细胞凋亡,这可能与启动许多凋亡相关基因的表达发生改变有相关,如fas家族基因、Bcl家族基因、c-fos基因、c-jun基因、核因子κB等。而缺血预处理可以通过减少细胞凋亡来减轻心肌缺血再灌注损伤的程度,这可能是抑制相关凋亡基因有关。全面了解这些基因表达改变及其意义,对于揭示缺血预处理的分子机制,从而进一步探索治疗心肌缺血再灌注损伤的分子靶具有重要意义。
Myocardial ischemia-reperfusion injury can induce cardiomyocyte apoptosis, which may be related to the initiation of many apoptosis related gene expression changes, such as fas family gene, Bcl family gene, c-fos gene, c-jun gene, nuclear factor κB and so on. Ischemic preconditioning can reduce myocardial ischemia-reperfusion injury by reducing apoptosis, which may be related to the inhibition of apoptosis-related genes. A comprehensive understanding of these changes in gene expression and its significance is of great importance for revealing the molecular mechanism of ischemic preconditioning and further exploration of molecular targets for the treatment of myocardial ischemia-reperfusion injury.