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 andMPO 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 CD_11b/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 CD_11b/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 CD_11b/CD₁₈.

Key words: triptolide, pancreatitis, respiratory distress syndrome, adult