【摘要】 目的:研究雷公藤内酯醇对重症急性胰腺炎肺损伤的保护作用及其可能作用机制。方法:36只雄性Wistar大鼠,随机分为3组,每组12只:假手术组(Sham组)、模型组(ALI组)和雷公藤内酯醇处理组(Tri组)。Sham组只行开腹术,ALI组和Tri组经胆胰管给予牛磺胆酸钠后,分别腹腔注射生理盐水、雷公藤内酯醇0.2 mg/kg。注射牛磺胆酸钠后6 h处死动物。每组中6只大鼠在处死前15 min静脉注射伊文思蓝(EB)20 mg/kg。测定支气管肺泡灌洗液(BALF)中髓过氧化物酶(MPO)活性和中性粒细胞(PMN)数。检测肺组织湿干重比(W/D)、EB含量、MPO活性、肺组织细胞间黏附分子1(ICAM-1)及PMN CD11b/CD18表达。观察肺组织病理学的改变。结果:与Sham组比较,ALI组肺组织病理学损伤严重,BALF中MPO、PMN水平和肺组织W/D、EB及MPO水平、ICAM-1及PMN CD11b/CD18表达水平升高(P<0.01);与ALI组比较,Tri组上述指标均降低(P<0.05或0.01)。结论:雷公藤内酯醇对重症急性胰腺炎肺损伤具有一定保护作用,与下调ICAM-1及PMNCD11b/CD18的表达进而抑制PMN在肺组织的聚集、激活有关。更多还原

【Abstract】 AIM: To investigate the effects of triptolide on severe acute pancreatitis-associated lung injury in rats and assess the possible mechanisms. METHODS: Thirty-six male Wistar rats were randomly divided into 3 groups(n=12): Sham,model and triptolide group.Sham group only underwent laparotomy.Immediately after undergoing retrograde intraductal injection of sodium taurocholate,triptolide and model groups received triptolide 0.2 mg/kg and normal saline,respectively.Six hours after sodium taurocholate injection,rats were sacrificed.Six animals in each group were intravenously injected with Evans blue(EB) 20 mg/kg at 15 min before sacrifice.Bronchoalveolar lavage fluid(BALF) was collected for determination of PMN count and MPO activity.The lungs were removed for evaluation of histological injury and determination of wet/dry lung weight(W/D) ratio,EB content,myeloperoxidase(MPO) activity,and expression levels of ICAM-1.The blood was obtained for determining the expression levels of PMN CD11b/CD18.The histopathologic changes of lung were observed.RESULTS: Compared with sham group,the histopathologic injury of lung in model group was serious,and the MPO activity,PMN count in BALF,the W/D ratio,EB content,MPO activity,the expression of ICAM-1 and PMN CD11b/CD18 in lung tissues were increased.Compared with model group,all of these changes were significantly reduced in triptolide group(P<0.05 or 0.01).CONCLUSION: Triptolide has protective effect against severe acute pancreatitis-associated lung injury in rats. The underlying mechanisms are via an inhibition of neutrophilic recruitment and activity through down-regulating the expressions of lung ICAM-1 and PMN CD11b/CD18.更多还原