烟雾吸入伤后大鼠肺内低分子磷脂酶A_2 mRNA表达与活性变化

The changes of mRNA expression and activity of pulmonary low molecular phospholipase A_2 in rats after smoke inhalation injury

目的 探讨大鼠肺内低分子磷脂酶A2 mRNA表达和酶活性变化与烟雾吸入性肺损伤的关系。方法 利用斑点杂交技术检测肺内低分子磷脂酶A2 (PLA2 Ⅰ、PLA2 Ⅱ )mRNA表达量、肺含水量及肺微血管通透性。结果 PLA2 ⅠmRNA表达式从伤后 1h开始下降 (从 2 7.37%降到 1 9.38% )、伤后 1 2h为 8.87% ,伤后 2 4h仍低于正常对照组 ;PLA2 ⅡmRNA表达从伤后 3h起持续增加 ,到伤后 2 4h与正常对照组的差值为 +1 1 0 .6 3% ;肺匀浆低分子磷脂酶 2活性从伤后 6h到伤后 2 4h持续性增加 ,并明显高于正常对照组 (P <0 .0 1 ) ;PaO2 从伤后 1h到伤后 2 4h均明显低于正常对照组 (P <0 .0 1 ) ,PaO2 在伤后 1 2h、2 4h明显低于正常对照组 (P<0 .0 1 ) ;肺组织含水量和碘 -1 3 1 (I-1 3 1 )白蛋白渗出量均从伤后 1h起明显增加 ,到伤后 6h达峰值 ,伤后 2 4h仍高于正常对照组 (P<0 .0 1 )。结论 PLA2 ⅡmRNA表达和低分子磷脂酶A2 活性增加参与了烟雾吸入性肺损伤的发生过程 ,并可能是引发多器官功能障碍的重要原因。

Objective To explore the relationship between the changes of mRNA and activity of pulmonary low molecular phospholipase A 2(PLA 2 Ⅰ,PLA 2 Ⅱ) and lung injury after smoke inhalation in rats.Methods The mRNA expressions of PLA 2 Ⅰ and PLA 2 Ⅱwere detected by blot hybridization,the activity of low molecular phospholipase A 2 in pulmonary homogenate was assayed with biochemistry, and simultaneously blood gases, lung water content and pulmonary microvascular permeability were measured.Results The expression of PLA 2 ⅠmMRNA had been decreased at 1h following smoke inhalation injury(from 27.37% to 19.38 %),the expression of PLA 2 ⅠmRNA was only 8.87% at 6h after injury and was still lower than it in control group at 24h after injury; The expression of PLA 2 ⅡmRNA was contineously enhanced from 3h to 24h following smoke inhalation injury and the expression of mRNA at 24h after injury exceeded +110.63% to it of control group; The activity of low molecular PLA 2 in pulmonary homogenate was significantly and contineously increased from 6h to 24h after injury compared with control group( P <0.01);PaO 2 was obviously decreased from 1h to 24h after injury compared with control group( P <0.01),but PaCO 2 at 12h and 24h following injury was remarkably higher than it in control group( P <0.01); lung water content and the exudation of I labeled albumin had been increased at 1h after injury and reached peak level at 6h after injury, and at 24h after injury it was significant higher while comparing to control group( P <0.01). Conclusion The expression of PLA 2 Ⅱ mRNA and the increase of molecular PLA 2 activity might participate in lung injury with smoke inhalation and lead to multiple organ dysfunction. Key words:low molecular phospholipase A 2 ;PLA 2 Ⅰ PLA 2 Ⅱ;lung smoke inhalation injury;rat