南昌大学学报（医学版）
南昌大學學報（醫學版）
남창대학학보（의학판）
ACTA ACADEMIAE MEDICINAE JIANGXI
2014年
3期
10-12,17
,共4页
丙泊酚%急性肺损伤%高迁移率族蛋白-1%动物,实验%大鼠
丙泊酚%急性肺損傷%高遷移率族蛋白-1%動物,實驗%大鼠
병박분%급성폐손상%고천이솔족단백-1%동물,실험%대서
propofol%acute lung injury%high mobility group box-1%animals,laboratory%rats
目的：探讨丙泊酚的肺保护作用及其可能作用机制。方法采用尾静脉注射内毒素建立急性肺损伤模型，丙泊酚和锌原卟啉同样经过尾静脉给药。将 Wistar 大鼠按随机数字表法分为实验对照组（C 组）、脂多糖组（L组）、脂多糖＋丙泊酚组（LP 组）。C 组尾静脉注射生理盐水；L 组尾静脉注射 LPS 7．5 mg·kg-1；LP 组尾静脉注射 LPS 7．5 mg·kg-1，同时静脉注射丙泊酚30 mg· kg-1。给药前及开始后第3、6和12 h 测定动脉血氧分压（PaO2），实验结束后观察肺湿/干重（W/D）比值、肺组织病理学检查并进行肺损伤轻重程度评分，同时观察各组大鼠肺组织高迁移率族蛋白1（HMGB-1）含量。结果实验前各组 PaO2无明显差异，注射 LPS 后 L 组 PaO2持续下降，和 C 组相比其 PaO2显著降低（P ＜0．05）。实验结束后 L 组和 C 组相比其 W/D 比值、肺组织病理学检查评分、HO-1及 HMGB-1含量显著增加（P ＜0．05）。而 LP 组和 L 组相比其 PaO2显著改善，而 W/D 比值、肺组织病理学检查评分及 HMGB-1含量显著降低（P ＜0．05）。结论丙泊酚具有肺保护作用，且该作用可能与其抑制 HMGB-1过度表达作用相关。
目的：探討丙泊酚的肺保護作用及其可能作用機製。方法採用尾靜脈註射內毒素建立急性肺損傷模型，丙泊酚和鋅原卟啉同樣經過尾靜脈給藥。將 Wistar 大鼠按隨機數字錶法分為實驗對照組（C 組）、脂多糖組（L組）、脂多糖＋丙泊酚組（LP 組）。C 組尾靜脈註射生理鹽水；L 組尾靜脈註射 LPS 7．5 mg·kg-1；LP 組尾靜脈註射 LPS 7．5 mg·kg-1，同時靜脈註射丙泊酚30 mg· kg-1。給藥前及開始後第3、6和12 h 測定動脈血氧分壓（PaO2），實驗結束後觀察肺濕/榦重（W/D）比值、肺組織病理學檢查併進行肺損傷輕重程度評分，同時觀察各組大鼠肺組織高遷移率族蛋白1（HMGB-1）含量。結果實驗前各組 PaO2無明顯差異，註射 LPS 後 L 組 PaO2持續下降，和 C 組相比其 PaO2顯著降低（P ＜0．05）。實驗結束後 L 組和 C 組相比其 W/D 比值、肺組織病理學檢查評分、HO-1及 HMGB-1含量顯著增加（P ＜0．05）。而 LP 組和 L 組相比其 PaO2顯著改善，而 W/D 比值、肺組織病理學檢查評分及 HMGB-1含量顯著降低（P ＜0．05）。結論丙泊酚具有肺保護作用，且該作用可能與其抑製 HMGB-1過度錶達作用相關。
목적：탐토병박분적폐보호작용급기가능작용궤제。방법채용미정맥주사내독소건립급성폐손상모형，병박분화자원계람동양경과미정맥급약。장 Wistar 대서안수궤수자표법분위실험대조조（C 조）、지다당조（L조）、지다당＋병박분조（LP 조）。C 조미정맥주사생리염수；L 조미정맥주사 LPS 7．5 mg·kg-1；LP 조미정맥주사 LPS 7．5 mg·kg-1，동시정맥주사병박분30 mg· kg-1。급약전급개시후제3、6화12 h 측정동맥혈양분압（PaO2），실험결속후관찰폐습/간중（W/D）비치、폐조직병이학검사병진행폐손상경중정도평분，동시관찰각조대서폐조직고천이솔족단백1（HMGB-1）함량。결과실험전각조 PaO2무명현차이，주사 LPS 후 L 조 PaO2지속하강，화 C 조상비기 PaO2현저강저（P ＜0．05）。실험결속후 L 조화 C 조상비기 W/D 비치、폐조직병이학검사평분、HO-1급 HMGB-1함량현저증가（P ＜0．05）。이 LP 조화 L 조상비기 PaO2현저개선，이 W/D 비치、폐조직병이학검사평분급 HMGB-1함량현저강저（P ＜0．05）。결론병박분구유폐보호작용，차해작용가능여기억제 HMGB-1과도표체작용상관。
Objective To investigate the protective effect of propofol on lung and its mecha-nism of action.Methods The endotoxin was injected into rats via the caudal vein to induce acute lung injury(ALI).The propofol and zinc protoporphyrin were also given via tail vein injection. The Wistar rats were randomly divided into three groups:control group(group C),lipopolysac-charide(LPS)group(group L),and LPS+propofol group(group LP).Saline solution was injected into rats of control group via caudal vein;lipopolysaccharide (7.5 mg· kg-1 )was injected into rats of LPS group via caudal vein;lipopolysaccharide (7.5 mg· kg-1 )and propofol (30 mg· kg-1 )were injected into rats of LPS+propofol group via caudal vein at the same time.The PaO2 was measured before and at 3,6 and 12 hours after treatment.Lung wet/dry weight ratio,lung in-jury score and high mobility group box-1(HMGB-1)expression were measured after the experi-ment.Results There were no significant differences in the PaO2 among the three groups before the experiment.After LPS injection,PaO2 in group L continuously decreased and was significantly lower than that in group C(P <0.05).After the experiment,lung wet/dry weight ratio,lung inju-ry score and HMGB-1 content in group L were significantly increased as compared with group C (P <0.05).Compared with group L,the PaO2 was obviously improved and lung wet/dry weight ratio,lung injury score and HMGB-1 content were significantly decreased in group LP(P <0.05). Conclusion Propofol can protect lung from endotoxin-induced acute lung injury through inhibi-ting the excessive expression of HMGB-1.
