| Objective:Actue lung injury (ALI) is a serious illness, the incidence and mortality are very high, although many researches on the mechanism and therapy of ALI are in progress, there are still no effective measures and specific medicines to treat it. Many researches indicated that the priming of inflammatory factors and apoptosis induced by PMN were the most two important mechanisms which caused ALI. To observe whether the AS has the protective effects against ALI and possible mechanism related to inflammatory factors and apoptosis, we set up the model of ALI induced by LPS. Methods: Balb/c mice were randomly divided into control, model, sham operation, model + vehicle, and model + Asiaticoside 5, 15, 45 mg.kg–1 groups. The mice model of ALI were established by intratracheal instillation of LPS 20μl(2.5 mg.kg-1). The sham operation group was given normal saline 20μl intratracheally . AS(5, 15 and 45 mg.kg-1) was administrated ig once a day for 3 days before the model of ALI was set up. Vehicle group was given ig 0.5% CMC. The others groups were ig normal saline. 24 h later, mice were killed, the lung, plasma, and BALF were collected to observe the change of lung specimen. The ratio of pulmonary wet weight to dry weight(W/D)was measured to estimate the extent of pulmonary edema.Lung pathological changes were also observed under the light microscope with hematoxylin and eosin staining. The protein expressions of COX-2 and HO-1 in lung tissue were analyzed by western- blot. The activity of MPO in lung was detected by MPO kit; the levels of PGE2 in plasma and IL-6, IL-10, TNF-αin BALF were detected by ELISA and the content of protein of BALF was detected by BCA . The apoptisis of PMN of BALF was detected by fluorescence microscope and the rate of apoptisis was detected by flow cytometry. Results and conclusion: (1) Obvious congestion of the lung tissue was found in both of model and vehicle groups with infiltration of polymorphologic cells , widen alveolar wall . The structure of pulmonary alveoli was demolished, hemorrhage and exudation of alveolar space was observed. These indicated that the model of ALI induced by LPS was succeed.,AS could alleviate damage of lung caused by LPS with decreased alveolar interstitial tissue edema, hemorrhage, and leucocyte infiltrationin in dose -dependent manner,(3)AS also reduced markedly content of IL-6, TNF-αof BALF, increased secretion of IL-10 of BALF, decreased content of PGE2 of plasma and the avtivity of MPO of lung, blunted expression of protein of COX-2 in lung, and elevated the protein expression of HO-1 in dose- dependent manner. These results indicate that AS can inhibite the injury of ALI induced by LPS through keeping the balance between inflammatory factors and anti-inflammatory factors. 4) AS promoted apoptosis of leucocytes, which might be related to improve the symptom of ALI and regression of inflammation.
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