丙泊酚对内毒素性急性肺损伤大鼠肺组织c-Jun氨基末端激酶活性的影响  

Propofol attenuates c-Jun terninal kinase activation in lipopolgsaccharides-induced acute lung injury in rats

作　　者：陈龙 成勤[3] 陈西艳 房孝梅 张茂银[2] 张稳稳[2] 刘功俭[2] 

机构地区：[1]徐州市第六人民医院麻醉科,221006 [2]徐州医学院附属医院麻醉科 [3]江苏省江门市人民医院麻醉科

出　　处：《国际麻醉学与复苏杂志》2011年第5期520-523,共4页International Journal of Anesthesiology and Resuscitation

基　　金：基金项目：江苏省“六大人才高峰”基金资助项目（06-B-065）;徐州市铜山区社会发展基金资助项目（TS005）

摘　　要：目的探讨大鼠内毒素性急性肺损伤（acute lung injury，ALI）时应用丙泊酚后处理对肺组织磷酸化c-Jun氨基末端激酶（phospho-c-Jun terninal kinnase，P-JNK）的影响。方法96只雄性SD大鼠按数字随机表法分为4组（每组24只）：生理盐水对照组（A组）；内毒素[有效成分为脂多糖（lipopolysaccharides，LPS）]致伤组5mg／kg尾静脉注射，B组）；丙泊酚低剂量治疗组（丙泊酚2mg／kg诱导后，4mg·kg-1·h-1维持，C组）；丙泊酚高剂量治疗组（丙泊酚4mg／kg诱导后，8mg·kg-1·h-1维持，D组）。每组大鼠均在诱导后1、2、3、4h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（westem-blot）和免疫组织化学法（immunocytoche-mical，IHC）检测肺组织c-Jun氨基末端激酶（c-Jun terninal kinase，JNK）磷酸化的水平。结果western-blot和IHC显示B、C、D3组各时点肺组织JNK磷酸化水平较A组均显著升高（P=0．02～0．03〈0．05或P=0．006～0．008〈0．01），3h时western-blot达到了322±32，比A组相同时点有显著升高（P=0．002〈0．01）；IHC显示P-JNK为21．7±4．4，比A组也有明显的增多（P=0．003〈0．01）。C组和D组大鼠的肺组织P-JNK与B组各时点相比有显著的降低（P=0．03—0．04〈0．05或P=-0．007～0．008〈0．01），western-blot显示3hP-JNK时分别下降到了235±26和179±21，而IHC则降低至15．1±3．1和12．3±1.7。D组P-JNK与c组相比，在诱导后3h也有显著地下降，其余各时点相比无统计学意义。结论丙泊酚可以显著抑制内毒素性ALI大鼠肺组织中P4NK的表达。Objective To investigate the effects of c-Jun terninal kinase （JNK） activation post-treated by propofol on lipopolysaccharide-induced acute lung injury. Methods Ninety six male SD rats were randomly divided into 4 equal groups （n=24） ： the control group（0.9% sodium chloride group）; Lipopolysaceharides （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 8 mg·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 c-Jun terninal kinase （p-JNK） was recorded in the lung tissues by the method of western-blot and Immunocytoehe-mical （IHC）. Results Western-blot and IHC shown that the activation of JNK in the lung tissues increased significantly after LPS administration （P=0.02-0.03〈0.05 or P=0.006-0.008〈0.01） . The number ofp-JNK was 322±32 and 21.7±4.4 shown by western-blot and IHC at the time point of 3 h after LPS administration. The p-JNK at all time points declined significantly after treatment with propofol in group C and group D and the p-JNK declined to 235±26 and 179±21（western-blot） and 15.1±3.1 and 12.3±1.7（IHC） at the time point of 3 h. Compared with group C, p-JNK declined more than those in group D at the time point of 3 h after after LPS administration. Conclusion Treatment with propofol can significantly attenuate the p-JNK expression in LPS- induced acute lung injury in rats.

关 键 词：丙泊酚 内毒素 急性肺损伤 C-JUN氨基末端激酶 

分 类 号：R614[医药卫生—麻醉学]