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在培养的乳鼠心肌细胞缺氧／复氧（A／R）模型上，观察缺氧预处理（APC）的细胞保护作用及其对细胞蛋白激酶C（PKC）活性和蛋白磷酸化的影响。结果表明，APC可减轻心肌细胞的H／R损伤：提高细胞存活率（P＜0．01），减少细胞脂质过氧化产物（MDA）生成（P＜0．01）及细胞内乳酸脱氢酶（LDH）和蛋白质的漏出（P＜0．01）。模拟APC的短暂缺氧（TA）显著激活PKC（125．0±11．2vs对照组52．1±8．4pmolPi／106cells，P＜0．01），使心肌细胞内分子量为66kD和31kD的蛋白条带32P掺入增加；PKC抑制剂H7完全消除APC对心肌细胞的保护作用，并抑制了短暂缺氧引起的PKC激活及蛋白磷酸化反应。磷酸酶抑制剂OA模拟，而激动剂BDM完全消除APC的保护作用；提示PKC介导了APC对心肌细胞的保护，其机理涉及PKC对其底物蛋白的磷酸化。
The effects of hypoxia preconditioning (APC) on cell protection and its effect on cell protein kinase C (PKC) activity and protein phosphorylation were observed on cultured neonatal rat cardiomyocytes hypoxia / reoxygenation (A / R) model. The results showed that APC can reduce H / R injury of cardiomyocytes: increase cell survival rate (P <0.01), decrease the production of lipid peroxidation product (MDA) (P <0.01) and intracellular lactate dehydrogenation Leakage of enzymes (LDH) and proteins (P <0.01). The transient hypoxia (TA) of mock APC significantly activated PKC (125.1 ± 8.4 vs 125 pmol / 106cells, P <0.01) in 125.0 ± 11.2 vs control group, and the intracellular contents of 66kD and 31kD Band 32P incorporation increased; PKC inhibitor H7 completely eliminate the protective effect of APC on cardiomyocytes, and inhibition of transient hypoxia-induced PKC activation and protein phosphorylation. Phosphatase inhibitor OA mimicry, and agonist BDM completely eliminate the protective effect of APC; prompted PKC mediated APC cardiomyocyte protection, the mechanism involved PKC substrate protein phosphorylation.