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从体外制备肾小管上皮细胞低氧、氧复苏模型入手，着重分析了低氧、氧复苏损伤过程中磷酯酶（ＰＬ）Ａ＿２的活性变化，ＰＬＡ＿２活性变化与细胞内钙稳态、脂质过氧化产物（ＬＰＯ）及ＰＧｓ、ＴｘＡ等脂类介质之间的关系，以探究低氧、氧复苏致肾小管上皮细胞损伤的本质。结果发现，在低氧及低氧、氧复苏时，ＰＬＡ＿２活性逐渐升高，尤其在氧复苏过程中，ＰＬＡ２活性升高明显；与此同时，［Ｃａ］ｉ自始至终处于高水平状态，两者呈明显相关关系（ｒ＝０．６８，Ｐ＜０．０１）。人为调节细胞外钙离子浓度也发现，Ｃａ浓度可明显影响ＰＬＡ＿２活性。ＰＬＡ＿２的激活呈明显Ｃａ依赖性。推测在低氧、氧复苏性损伤中，ＰＬＡ＿２的激活极有可能是由于低氧、氧复苏造成的细胞内钙离子浓度增高所致。ＰＬＡ＿２的损伤作用可能与由其引起的脂质过氧化及脂类介质的产生与释放有关。ＣｙＡ可明显阻断ＰＬＡ＿２的激活以及过氧化脂质、脂类介质的大量产生和堆积，缓解低氧、氧复苏所造成的细胞损伤。
The model of tubular epithelial cell hypoxia and oxygen resuscitation was established in vitro. The changes of phospholipase (A 2 A) activity during hypoxia and oxygen resuscitation were analyzed. The changes of PLA 2 activity and the intracellular calcium homeostasis, Oxidation products (LPO) and PGs, TxA and other lipid media to explore the nature of hypoxic and oxygen-induced renal tubular epithelial cell injury. The results showed that the activities of PLA 2 increased gradually during hypoxia and hypoxia and oxygen resuscitation, especially during the process of oxygen resuscitation. Meanwhile, [Ca] i was high from beginning to end, Significant correlation (r = 0.68, P <0.01). Man-made regulation of extracellular calcium concentration also found that Ca concentration can significantly affect PLA 2 activity. Activation of PLA 2 showed obvious Ca-dependent. Speculated that in hypoxia, oxygen resuscitation injury, PLA2 activation is most likely due to hypoxia, oxygen recovery caused by increased intracellular calcium ion concentration. The damage of PLA_2 may be related to the lipid peroxidation and the production and release of lipid mediators. CyA can obviously block the activation of PLA 2 and the massive production and accumulation of lipid peroxides and lipid mediators and alleviate the cell injury caused by hypoxia and oxygen resuscitation.