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心脏的缺血/再灌注可引起核转录因子(NF kB)活化,促使细胞因子、粘附分子及趋化因子等促炎性因子的过度表达,而这些因子均可直接或间接造成心肌的炎症损伤。抗氧化剂PDTC作为NF kB的抑制剂,能有效抑制它的活化[1] 。此外,大量的实验研究证明,钾通道开放剂(KCOs)所产生的超极化
Cardiac ischemia / reperfusion induces nuclear factor kB (NF kB) activation and promotes the overexpression of proinflammatory cytokines, such as cytokines, adhesion molecules and chemokines, which directly or indirectly contribute to myocardial inflammation damage. Antioxidant PDTC acts as an inhibitor of NF kB and effectively inhibits its activation [1]. In addition, a large number of experimental studies have demonstrated that potassium channel openers (KCOs) produce hyperpolarization