Department of Cardiac Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Biomed Res Int. 2019 Jul 16;2019:7587451. doi: 10.1155/2019/7587451. eCollection 2019.
Nowadays, the prevention of severe myocardium injury resulting from myocardial ischemia/reperfusion injury (I/R) has been recognized as an important subject in the field of ischemic heart disease. In this study, H9c2 cardiomyocytes were exposed to cycles of hypoxia/reoxygenation (H/R) to mimic myocardial I/R injury. Western blot analysis and qRT-PCR were performed to detect the expression of Cox-2, Akt and p-Akt. Cell viability, LDH release and activity of Caspase-3 were assessed to determine the protective effect of propofol. The results proved that the protective effect of propofol for H/R challenged cardiomyocytes was associated with Akt phosphorylation. We also revealed that treatment of propofol suppressed the expression of Cox-2 in cardiomyocytes which was up-regulated after H/R treatment. Conversely, the over-expression of Cox-2 inhibited Akt phosphorylation while enhancing cardiomyocytes apoptosis. Interestingly, Akt activator exhibited similar protective effect with propofol and could diminish the influences brought by over-expression of Cox-2. Thus, it could be concluded that Cox-2 negatively affects the protective effect of propofol against hypoxia/reoxygenation induced cardiomyocyte apoptosis by suppressing Akt phosphorylation.
如今，预防心肌缺血/再灌注损伤（I/R）导致的严重心肌损伤已被认为是缺血性心脏病领域的一个重要课题。在这项研究中，使用 H9c2 心肌细胞进行缺氧/复氧（H/R）循环处理来模拟心肌 I/R 损伤。通过 Western blot 分析和 qRT-PCR 检测 Cox-2、Akt 和 p-Akt 的表达。通过评估细胞活力、LDH 释放和 Caspase-3 的活性来确定异丙酚的保护作用。结果证明，异丙酚对 H/R 刺激的心肌细胞的保护作用与 Akt 磷酸化有关。我们还揭示，异丙酚处理抑制了 Cox-2 在心肌细胞中的表达，Cox-2 在 H/R 处理后上调。相反，Cox-2 的过表达抑制了 Akt 磷酸化，同时增强了心肌细胞凋亡。有趣的是，Akt 激活剂表现出与异丙酚相似的保护作用，并可以减轻 Cox-2 过表达带来的影响。因此，可以得出结论，Cox-2 通过抑制 Akt 磷酸化对异丙酚预防缺氧/复氧诱导的心肌细胞凋亡的保护作用产生负面影响。
