Hoshida Shiro, Yamashita Nobushige, Otsu Kinya, Hori Masatsugu
Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan.
Cardiovasc Res. 2002 Aug 15;55(3):495-505. doi: 10.1016/s0008-6363(02)00337-1.
It is clinically important to elucidate the mechanism underlying the delayed preconditioning against ischemia-reperfusion injury observed 24-72 h after sublethal stress such as brief ischemia, hyperthermia and exercise. The time course of induction of myocardial manganese-superoxide dismutase (Mn-SOD) and appearance of the ischemic tolerance coincide well, and the percent increase in Mn-SOD activity and percent reduction of infarct size are correlated well under various stresses. Furthermore, treatments with antisense oligodeoxynucleotides to Mn-SOD completely abolished the delayed preconditioning and any increase in Mn-SOD content. These results indicate that Mn-SOD induction plays a pivotal role in the late phase preconditioning afforded with brief ischemia, hyperthermia and exercise. We also showed that cytokines, e.g., tumor necrosis factor-alpha and interleukin-1beta, and reactive oxygen species are involved in the process of signal transduction for the Mn-SOD induction.
阐明诸如短暂缺血、热疗和运动等亚致死性应激后24 - 72小时观察到的延迟预处理对抗缺血再灌注损伤的潜在机制具有临床重要性。心肌锰超氧化物歧化酶（Mn - SOD）诱导的时间进程与缺血耐受性的出现吻合良好，并且在各种应激下，Mn - SOD活性的百分比增加与梗死面积的百分比减少密切相关。此外，用针对Mn - SOD的反义寡脱氧核苷酸处理完全消除了延迟预处理以及Mn - SOD含量的任何增加。这些结果表明，Mn - SOD诱导在短暂缺血、热疗和运动所提供的晚期预处理中起关键作用。我们还表明，细胞因子，如肿瘤坏死因子 - α和白细胞介素 - 1β，以及活性氧参与了Mn - SOD诱导的信号转导过程。
