Abstract: Abstract Objective: To explore the effects of sodium aescinate(SA) on p38 mitogen-activated protein kinase(p38MAPK) signal transduction pathway in lung injury induced by intestinal ischemia reperfusion. Methods: 24 SD rats were randomly divided into three groups:sham group,IR group,treatment group. In sham group ,superior mesenteric artery was separated only; Models of intestinal IR injury were estabished with clamping of the superior mesenteric artery for 1h and then clamping was relieved for 1h. In treatment group, SA(0.9μg/g) was injected through tail vein before ischemia, before reperfusion and after reperfusion 30min respectively. Pulmonary surfactant(PS), lung wet/dry weight ratio, xanthine oxidase(XOD), malondialdehyde(MDA) , myeloperoxidase (MPO) in plasma and lung tissue were measured, as well as the expression levels of p38MAPK and Bax proteins in lung tissue were examined using immunohistochemical method. Results: (1) In IR group, PS were significently decreased than that in sham group(P<0.01), and while lung wet/dry weight ratio were significantly increased than that in sham group(P<0.01), The above-mentioned indexes of treatment group were obviously ameliorated in comparison with IR group(P<0.01).(2) The activity of ,XOD,MPO and the content of MDA in in plasma and lung tissue were significently increased in IR group than that in sham group (P<0.01). The above-mentioned indexes of treatment group were obviously lower in comparison with IR group(P<0.01). (3)The protein expression level of p38MAPK and Bax were significantly increased in IR group than that in sham group and treatment group(P<0.01).(4)The correlation analysis indicated that MDA,MPO and the expression levels of Bax proteins in lung tissue were positively correlated with the expression levels of p38MAPK proteins(P<0.01). Conclusion: Sodium aescinate can prevent the lung injury induced by intestinal ischemia reperfusion(IR) ,such protective effect may be related to the adjustment of the p38MAPK signal transduction pathway by inhibiting the generation of oxygen free radicals and activation of neutrophils and then prevent apoptosis.

Key words: reperfusion injury escin p38 mitogen-activated protein kinases respiratory distress syndrome, adult lecithins phospholipidsxanthine oxidase malondialdehyde, 黄嘌呤氧化酶