摘要
【摘要】目的探讨急性呼吸窘迫综合征（ARDS）时血小板活化的信号通路。方法将30只健康sD大鼠按随机数字表法分为对照组（n=6）和模型组（n=24）。采用经尾静脉注射油酸0．25mL／kg制备ARDS模型；对照组给予等量生理盐水。模型组于制模后2、6、24、72h取腹主动脉血，分离血小板，采用蛋白质免疫印迹试验（WestemB10t）检测血小板丝裂素活化蛋白激酶（MAPKs）通路中的主要蛋白激酶c—Jun氨基末端蛋白激酶（JNK）的磷酸化（pJNK）水平；处死动物取肺组织，计算肺系数（肺质量，体质量×100％）及肺湿／干质量（W／D）比值；苏木素一伊红（HE）染色后，光镜下观察肺组织病理学变化。结果与对照组相比，ARDS模型组大鼠制模后2h血小板vJNS：水平即明显增高（灰度值：0．72±O．09比0．22±0．01），6h达峰值（灰度值：0．91±0．03比0．22±0．01），之后逐渐降低，至72h仍明显高于对照组（灰度值：0．39±0．06比0．22±0．0l，均P〈0．05）。ARDS模型组大鼠制模后2h大鼠肺系数和肺W／D比值即较对照组明显升高[分别为（1．30±0．20）％比（0．60±0．10）％、6．00±0．60比3．30±0．30]，之后随时间延长逐渐降低，但直至72h肺系数和肺W／D比值仍明显高于对照组[分别为（0．90±0．10）％比（0．60±0．10）％、4．80±0．70比3．30±0．30，均P〈0．05]。光镜下显示，对照组大鼠肺组织无明显病理学改变。模型组制模后2h即可见明显的肺泡水肿和间质水肿，炎性细胞浸润，小血管扩张、充血，肺泡内有大量蛋白渗出物；24h病变达极期；72h肺泡腔液体渗出大部分被吸收，肺泡腔缩小，肺泡间隔增厚，炎性细胞浸润减轻，纤维组织增生，有微血栓形成。结论ARDS时肺组织除发生病理学改变外，血小板也发生了活化，且其活化过程与JNK信号转导通路启动有关。
Objective To investigate the signal pathway of platelet activation in acute respiratory distress syndrome （ARDS）. Methods Thirty healthy Sprague-Dawley （SD） rats were randomly divided into control group （n = 6） and model group （n = 24）. The model of ARDS was reproduced by intravenous injection of oleic acid （0.25 mL/kg）, and the rats in control group were injected with the same amount of normal saline. The blood of abdominal aorta was collected at 2, 6, 24, and 72 hours after model reproduction, the platelets were separated, and c-Jun N-terminal kinase phosphorylation （pJNK） levels which was one of major protein kinases in the mitogen-activated protein kinases （MAPKs） signal pathway was determined by Western Blot. The rats were sacrificed, the lung tissues were harvested, and lung coefficient （lung weight/body weight X 100%） and lung wet/dry （W/D） ratio were calculated. Pathological changes in the lung tissue were observed with hematoxylin-eosin （HE） staining in light microscope. Results Compared with the control group, platelet pJNK level in ARDS model group was significantly increased at 2 hours after model reproduction （gray value： 0.72 ± 0.09 vs. 0.22±0.01）, and peaked at 6 hours （gray value： 0.91 ±0.03 vs. 0.22±0.01）, then it was decreased gradually. It was also significantly higher than that of control group till 72 hours after model reproduction （gray value： 0.39 ± 0.06 vs. 0.22±0.01, all P 〈 0.05）. Lung coefficient and lung W/D ratio in ARDS model group were significantly increased at 2 hours after model reproduction as compared with those of control group [（1.30 ± 0.20）% vs. （0.60 ±_ 0.10）%, 6.00 ± 0.60 vs. 3.30±0.30], then they were decreased gradually. They were also significantly higher than those of control group till 72 hours after model reproduction [（0.90±0.10）% vs. （0.60±0.10）%, 4.80±0.70 vs. 3.30±0.30, all P 〈 0.05]. It was showed by light microscopy that lung tissue of rats in the control group had no si
出处
《中华危重病急救医学》
CAS
CSCD
北大核心
2016年第6期553-556,共4页
Chinese Critical Care Medicine
基金
山西省自然科学基金（2013011055-5）
山西省大同市基础研究计划项目（2014105-2）
