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目的探讨蛋白激酶Ｃ（ＰＫＣ）在心脏以外组织器官缺血或缺氧预处理（ＰＣ）保护中的作用及其机理。方法分别在原位灌流的大鼠小肠、肢体缺血再灌注模型和培养的大鼠胸主动脉血管平滑肌细胞（ＶＳＭＣ）缺氧复氧模型上观察ＰＫＣ对于器官缺血或细胞缺氧ＰＣ作用的影响。结果ＰＫＣ抑制剂Ｈ７和多粘菌素Ｂ完全消除缺血ＰＣ对小肠和肢体的保护作用；缺氧ＰＣ激活ＶＳＭＣ内ＰＫＣ，并使ＰＫＣ介导的蛋白磷酸化反应加强。结论ＰＫＣ激活是心脏以外组织器官ＰＣ保护的重要环节，其机制可能与底物蛋白的磷酸化有关。
Objective To investigate the role and mechanism of protein kinase C (PKC) in the protection of ischemic or hypoxic preconditioning (PC) in tissues other than the heart. Methods The effect of PKC on organ ischemia or hypoxic PC was observed in rat intestinal perfused rat models, limb ischemia-reperfusion models and cultured rat aorta vascular smooth muscle cells (VSMCs) model of hypoxia-reoxygenation influences. Results PKC inhibitor H7 and polymyxin B completely abolished the protective effect of ischemic PC on small intestine and limb. Anoxia PC activated PKC in VSMC and enhanced PKC-mediated phosphorylation. Conclusion Activation of PKC is an important part of PC protection in tissues and organs other than the heart. Its mechanism may be related to the phosphorylation of substrate protein.