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目的 观察在整体炎症过程中炎症白细胞磷脂酶D(PLD)活性的变化和炎症的关系。方法 采用大鼠角叉菜胶胸膜炎模型 ,以渗出液量和细胞数及渗出液中髓过氧化物酶活性 (中性粒细胞脱颗粒指标 )作为炎症程度。用酶偶联比色法测定白细胞PLD活性。结果 正常大鼠外周血白细胞PLD活性极低 ,为 ( 0 14± 0 0 3) μmol·g-1·min-1。致炎后各时间点胸膜腔渗出白细胞的PLD活性明显升高 ,分别可达 40～ 6 0倍 ,并在 3h达峰值 ,明显早于炎症高峰 ( 12h)。不同剂量 ( 5 0 0 μg和 10 0 0 μg)角叉菜胶可引起致炎 12h明显不同程度的炎症 ,但渗出白细胞PLD活性两者差别不大。低剂量吲哚美辛 ( 2mg·kg-1,ip)和地塞米松 ( 0 1mg·kg-1,ip)均明显抑制致炎 6h大鼠胸膜腔的渗出 ,但渗出白细胞PLD活性与对照组相比差别无显著性。结论 大鼠角叉菜胶性胸膜炎白细胞PLD活性显著升高 ,提示PLD活性升高在该炎症模型中是原发性表现 ,低剂量吲哚美辛和地塞米松的抗炎机制与PLD无关
Objective To observe the relationship between the changes of inflammatory leukocyte phospholipase D (PLD) activity and inflammation during the whole inflammatory process. Methods The carrageenin pleuritis model was used in rats. The amount of exudate, the number of cells and the activity of myeloperoxidase in the exudate (neutrophil degranulation index) were used as the inflammation degree. Leucocyte PLD Activity Measured by Enzyme Coupled Colorimetry. Results The PLD activity of peripheral blood leukocytes in normal rats was extremely low (0 14 ± 0 0 3) μmol · g-1 · min-1. PLD activity in pleural effusion leukocytes at each time point after inflammation was significantly higher, reaching 40 ~ 60 times respectively, reaching the peak value at 3h and obviously earlier than the peak of inflammation (12h). Carrageenan at different dosages (500 μg and 100 μg) caused a markedly different degree of inflammation at 12h, but there was no obvious difference in PLD activity between leukocytes and leukocytes. Low doses of indometacin (2 mg · kg-1, ip) and dexamethasone (0 1 mg · kg-1, ip) significantly inhibited the exudation of the pleural cavity in rats with inflammatory 6h, but the exudative leukocyte PLD activity and The difference between the control group was not significant. Conclusion The PLD activity of rat leucocephalus was significantly increased in rats, suggesting that PLD activity was the primary manifestation in this inflammatory model. The anti-inflammatory mechanism of low dose indomethacin and dexamethasone was not related to PLD