医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2014年
6期
718-721
,共4页
林雪松%向军%蔡亚娜%汪乐
林雪鬆%嚮軍%蔡亞娜%汪樂
림설송%향군%채아나%왕악
乌司他丁%损伤,肺,急性%内毒素%水通道蛋白
烏司他丁%損傷,肺,急性%內毒素%水通道蛋白
오사타정%손상,폐,급성%내독소%수통도단백
Ulinastatin%Injury,lung,acute%Endotoxin%Aquaporin
目的：探讨乌司他丁对急性内毒素性肺损伤保护作用的机制。方法取SD大鼠20只，大鼠腹腔注射脂多糖（ LPS）5 mg·kg-1·d-1，按随机数字表法将大鼠分配进入乌司他丁组和对照组各10只。乌司他丁组静脉给予乌司他丁50 kU·kg-1，对照组给予等量0.9％氯化钠溶液，观察大鼠水通道蛋白-1（AQP-1），AQP-5的表达变化及肺泡壁厚度变化以及肺水肿的程度。结果对照组大鼠体内注射LPS后，AQP-1及AQP-5的表达持续性降低，乌司他丁组AQP-1及AQP-5降低不明显；对照组肺组织湿/干质量比值明显增高，乌司他丁组无明显变化。对照组24，48，72 h的肺泡壁厚度（3.84±0.68），（6.32±1.08），（11.03±2.47）μm，乌司他丁组分别为（2.31±0.44），（3.76±0.82），（2.94±0.67）μm，无明显变化。结论 AQP-1及AQP-5通过调节细胞通透性而导致肺水肿，乌司他丁通过减缓上述过程从而减轻内毒素性肺损伤的程度。
目的：探討烏司他丁對急性內毒素性肺損傷保護作用的機製。方法取SD大鼠20隻，大鼠腹腔註射脂多糖（ LPS）5 mg·kg-1·d-1，按隨機數字錶法將大鼠分配進入烏司他丁組和對照組各10隻。烏司他丁組靜脈給予烏司他丁50 kU·kg-1，對照組給予等量0.9％氯化鈉溶液，觀察大鼠水通道蛋白-1（AQP-1），AQP-5的錶達變化及肺泡壁厚度變化以及肺水腫的程度。結果對照組大鼠體內註射LPS後，AQP-1及AQP-5的錶達持續性降低，烏司他丁組AQP-1及AQP-5降低不明顯；對照組肺組織濕/榦質量比值明顯增高，烏司他丁組無明顯變化。對照組24，48，72 h的肺泡壁厚度（3.84±0.68），（6.32±1.08），（11.03±2.47）μm，烏司他丁組分彆為（2.31±0.44），（3.76±0.82），（2.94±0.67）μm，無明顯變化。結論 AQP-1及AQP-5通過調節細胞通透性而導緻肺水腫，烏司他丁通過減緩上述過程從而減輕內毒素性肺損傷的程度。
목적：탐토오사타정대급성내독소성폐손상보호작용적궤제。방법취SD대서20지，대서복강주사지다당（ LPS）5 mg·kg-1·d-1，안수궤수자표법장대서분배진입오사타정조화대조조각10지。오사타정조정맥급여오사타정50 kU·kg-1，대조조급여등량0.9％록화납용액，관찰대서수통도단백-1（AQP-1），AQP-5적표체변화급폐포벽후도변화이급폐수종적정도。결과대조조대서체내주사LPS후，AQP-1급AQP-5적표체지속성강저，오사타정조AQP-1급AQP-5강저불명현；대조조폐조직습/간질량비치명현증고，오사타정조무명현변화。대조조24，48，72 h적폐포벽후도（3.84±0.68），（6.32±1.08），（11.03±2.47）μm，오사타정조분별위（2.31±0.44），（3.76±0.82），（2.94±0.67）μm，무명현변화。결론 AQP-1급AQP-5통과조절세포통투성이도치폐수종，오사타정통과감완상술과정종이감경내독소성폐손상적정도。
Objective To investigate the protection mechanism of ulinastatin on bacterial endotoxin-induced acute lung injury. Methods Acute lung injury was induced by Escherichia colilipo-polysaccharide(LPS)5 mg·kg-1·d-1,intratracheally. Twenty SD rats were randomly divided into control group(n=10)and ulinastatin group(n=10). Ulinastatid group received ulinastatin 50 kU·kg-1 ,the control groups received the same amount of 0. 9% sodium chloride solution. Then the expression changes of rat AQP-1 and AQP-5,alveolar wall thickness change and the degree of pulmonary edema were detected. Results After the injection of LPS into the rat,the expression of AQP-1 and AQP-5 in control group were continuously decreased,but those in ulinastatin group decreased were not obvious. The lung wet/dry weight ratio in the control group increased significantly,the not obvious changes in the ulinastain group. The thickness of the alveolar in 24,48,72 h of the control group were(3. 84±0. 68),(6. 32±1. 08),(11. 03±2. 47)μm, respectively,and those in the ulinastian groups were(2. 31±0. 44)(,3. 76±0. 82)(,2. 94±0. 67)μm,respectively. Conclusion The AQP-1 and AQP-5 induced the occurrence of pulmonary edema by changing the cell permeability. Ulinastatin can slow down the process so as to reduce the degree of endotoxin-induced lung injury.
