中文摘要：

目的 探讨重症急性胰腺炎（SAP）诱发急性肺损伤（ALI）时肺组织Ⅱ型分泌型磷脂酶A2（sPLA2-Ⅱ）的表达及清胰汤的干预作用.方法 将30只SD大鼠按随机数字表法分为假手术组、模型组、清胰汤干预组,每组10只.采用胰胆管逆行注射去氧胆酸钠建立SAP诱发ALI模型;假手术组仅剖腹翻动胰腺.清胰汤组于制模后30 min和12 h分别给予清胰汤10 ml/kg灌胃.术后24 h各组进行血气分析,测定血清淀粉酶、sPLA2含量及肺组织湿/干重（W/D）比值;采用逆转录-聚合酶链反应（RT-PCR）、蛋白质免疫印迹法（Western blotting）测定肺组织sPLA2-Ⅱ的mRNA和蛋白表达,并观察肺、胰组织病理变化.结果 与假手术组比较,模型组动脉血氧分压（PaO2）、pH值显著降低[PaO2（mm Hg,1 mm Hg=0.133 kPa）：79.24±5.84比96.78±3.81,pH值：7.269±0.054比7.391±0.054],动脉血二氧化碳分压（PaCO2）、血清淀粉酶、肺W/D比值、血sPLA2显著升高[PaCO2（mm Hg）：47.57±2.55比27.69±1.02,血清淀粉酶（U/L）：7 144.19±727.91比1 193.41±192.54,肺W/D 比值：8.57±2.45比3.70±0.90,血sPLA2（nmol·min^-1·ml^-1）：45.13±6.0比29.94±6.39],肺sPLA2-ⅡmRNA（1.28±0.21比0.80±0.08）和蛋白表达显著升高（均P〈0.05）.与模型组比较,清胰汤组PaO2、pH值明显升高[PaO2：（88.16±5.07） mm Hg,pH值：7.322±0.039],PaCO2、血清淀粉酶、肺W/D比值、血sPLA2明显降低[PaCO2：（33.13±2.14） mm Hg,血清淀粉酶：（4 283.51±527.52） U/L,肺W/D比值：4.05±0.52,血sPLA2：（28.00±4.78） nmol·min^-1·ml^-1],且肺sPLA2-ⅡmRNA（0.89±0.08）和蛋白表达显著降低（均P〈0.05）.清胰汤组肺、胰组织病理改变较模型组明显减轻.结论 SAP时肺组织sPLA2-Ⅱ表达增高可能是ALI的发病机制之一;清胰汤可能在转录水平抑制sPLA2-Ⅱ的表达,从而保护肺功能.

英文摘要：

Objective To investigate the expression of secretory type Ⅱ phospholipase A2 （sPLA2-Ⅱ） in lung of rats with acute lung injury （ALI） complicating severe acute pancreatitis （SAP）, and the effect of Qingyi decoction （QYT, 清胰汤） on ALI. Methods Thirty Sprague Dawley （SD） rats were randomly divided into three groups： sham operation （SO） group, model group and QYT group, with 10 rats in each group. SAP model was reproduced by reverse injection of sodium deoxycholate into the common bile-pancreatic duct of rats. The pancreas of rats was just exposed in SO group. QYT （10 ml/kg） was gavaged 30 minutes and 12 hours after SAP was induced in QYT group. The blood gas analysis was performed 24 hours after operation. Serum amylase （AMY） levels, sPLA2 and lung wet/dry ratio （W/D） were determined. The sPLA2-Ⅱ mRNA and sPLA2-Ⅱ protein expression in lung were detected by reverse transcription-polymerase chain reaction （RT-PCR） and Western blotting. The pathological changes in lung and pancreas were observed. Results Compared with SO group, the levels of arterial partial pressure of oxygen （PaO2） and pH value in model group were significantly decreased [PaO2 （mm Hg, 1 mm Hg=0.133 kPa）： 79.24±5.84 vs. 96.78±3.81, pH value： 7.269±0.054 vs. 7.391±0.054], arterial partial pressure of carbon dioxide （PaCO2）, the serum levels of AMY, W/D ratio and the serum levels of sPLA2 were significantly increased [PaCO2 （mm Hg）： 47.57±2.55 vs. 27.69±1.02, AMY （U/L）： 7 144.19±727.91 vs. 1 193.41±192.54, W/D ratio： 8.57±2.45 vs. 3.70±0.90, sPLA2 （nmol·min^-1·ml^-1）： 45.13±6.05 vs. 29.94±6.39], the expression of sPLA2-Ⅱ mRNA （1.28±0.21 vs. 0.80±0.08） and protein were significantly increased （all P〈0.05）. Compared with model group, blood PaO2 and pH value were significantly increased [PaO2： （88.16±5.07） mm Hg, pH value： 7.322±0.039], the PaCO2, the serum levels of AMY, W/D ratio and the serum levels of sPLA2 in QYT group were s