国际麻醉学与复苏杂志   2011, Issue (5): 520-523
    
丙泊酚对内毒素性急性肺损伤大鼠肺组织JNK活性的影响
陈龙, 陈西艳, 房孝梅, 张茂银, 成勤, 张稳稳, 刘功俭1()
1.徐州市第六人民医院
Propofol attenuates JNK activation in LPS-induced Acute Lung Injury in rats
 全文:
摘要:

目的 探讨大鼠内毒素性急性肺损伤时应用丙泊酚后处理对肺组织p-JNK的影响。方法96只雄性SD大鼠按数字随机表随机分为4组,每组24只。生理盐水对照组(A组);内毒素致伤组(LPS 5 mg/kg 尾静脉注射,B组);丙泊酚低剂量治疗组(丙泊酚2 mg/kg诱导后,4 mg﹒kg-1﹒h-1 维持,C组);丙泊酚高剂量治疗组(丙泊酚4 mg/kg诱导后,8 mg﹒kg-1﹒h-1 维持,D组)。每组大鼠均在诱导后1、2、3、4 h时经放血处死大鼠(采用放血法随机活杀6只大鼠并留取肺组织标本),用免疫蛋白印迹法(western-blot)和免疫组织化学法(IHC)检测肺组织JNK磷酸化的水平。结果B组在LPS注射后各时点肺组织JNK磷酸化水平均较A组显著升高( P<0.05或P<0.01),尤以3 h时最为显著(P=0.002<0.01),而在应用丙泊酚处理后,虽然大鼠的肺组织JNK磷酸化水平也较A组同时点相比有显著的升高( P<0.05和P<0.01),但和B组相比却有显著的降低(P<0.05或P<0.01),在3h时降低最为明显(P=0.008<0.01)。结论 丙泊酚可以显著抑制内毒素性急性肺损伤大鼠肺组织中p-JNK的表达。显。结论 丙泊酚可以显著抑制内毒素性急性肺损伤大鼠肺组织中p-JNK的表达。

关键词: 丙泊酚;内毒素;肺损伤;c-Jun氨基末端激酶(JNK)
Abstract:

Objective: To investigate the effects of JNK activation posttreated by propofol on lipopolysaccharide-induced acute lung injury. Methods: 96 male SD rats were randomly devided into 4 equal groups (n=24), namely the control group(0.9% sodium chloride group); LPS group (intravenous injection of LPS 5 mg/kg); low dose of propofol group (2 mg/kg induced and 4 mg﹒kg-1﹒h-1 maintained); large dose of propofol group (4 mg/kg induced and 8mg﹒kg-1﹒h-1 maintained). Six rats were killed at each time point after LPS intravenous administration(saline in group A)and the lungs were harved and the activation of Phospho-JNK (p-JNK) was recorded in the lung tissues by the method of western-blot and Immunocytoche-mical (IHC). Results: The activation of p-JNK in the lung tissues increasecd significantly after LPS administration( P<0.05orP<0.01) and at the time point of 3 h after after LPS administration the increasing was most(P=0.002<0.01) ,but declined significantly after treatment with propofol and the activation of p-JNK in group D declined more than those in group C (P<0.05orP<0.01) and at the time point of 3 h after after LPS administration the degression was most(P=0.008<0.01). Conclusions: Treatment with propofol can significantly attenuate the p-JNK expression in LPS-induced acute lung injury in rats.

Key words: Propofol;Endotoxin;Acute lung injury;C-Jun terninal kinase(JNK)