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目的:研究荆防散正丁醇部位对LPS所致急性肺损伤(ALI)模型小鼠的保护作用及其可能机制。方法:将小鼠分为空白对照组、假手术组、LPS模型组、LPS+地塞米松(5 mg/kg)组、LPS+荆防散正丁醇部位组(3.33、6.67、10.01 g/kg),除地塞米松组小鼠于第2、4、5天各腹腔注射给药1次外,其余各组小鼠均连续ig给药5d,1次/d,第5天给药30 min后,除空白组小鼠不作任何处理、假手术组气管滴注等容积无菌生理盐水外,其余各组小鼠均气管滴注LPS 100μL(5 mg/kg)制备ALI模型,所有动物于处死前1 h再给药1次。滴注LPS 6 h后,处死小鼠,收集肺泡灌洗液(BALF),剖取小鼠肺脏,测定小鼠肺湿干重比值(W/D)与肺指数;比色法测定BALF中总蛋白含量及肺组织MPO活性,ELISA法测定BALF中IL-6、IL-1β、TNF-α及趋化因子MIP-1α、MIP-1γ含量。结果:荆防散正丁醇部位(6.67 g/kg)能降低ALI小鼠BALF中总蛋白含量,明显降低肺W/D与肺指数,降低肺组织MPO活性;同时该部位能显著降低BALF中促炎细胞因子IL-6、IL-1β、TNF-α及趋化因子MIP-1α、MIP-1γ水平。结论:荆防散正丁醇部位对ALI小鼠有一定保护作用,能减轻肺水肿,减轻肺部炎性反应,作用机制与抑制炎症细胞因子释放有关。
Objective: To study the protective effect of Jing-Fang-San n-butanol fraction on acute lung injury (ALI) induced by LPS in mice and its possible mechanism. Methods: The mice were divided into blank control group, sham operation group, LPS model group, LPS + dexamethasone (5 mg / kg) group, LPS + Jingban San n-butanol group (3.33,6.67,10.01 g / , Except for the dexamethasone group mice were injected intraperitoneally on the 1st, 2nd, 5th and 5th day for 1 time. The other mice in each group were given ig for 5 days, once a day for 30 minutes , The mice in each group were given tracheal instillation of LPS 100 μL (5 mg / kg) to prepare ALI model except the blank group mice without any treatment. 1 h and then given 1 time. The mice were sacrificed 6 h after LPS instillation, BALF was collected, the lungs of mice were taken out and the W / D ratio and lung index were measured. The total BALF The contents of IL-6, IL-1β, TNF-α and chemokines MIP-1α and MIP-1γ in BALF were measured by ELISA. Results: The n-butanol fraction (6.67 g / kg) could reduce the total protein in BALF of ALI mice and significantly decrease the lung W / D and pulmonary index, and decrease the activity of MPO in lung tissue. In the meantime, Pro-inflammatory cytokines IL-6, IL-1β, TNF-α and chemokines MIP-1α, MIP-1γ levels. CONCLUSION: Jing-Fang-San n-butanol fraction has a protective effect on ALI mice and can reduce pulmonary edema and lung inflammatory response, the mechanism of which is related to the inhibition of the release of inflammatory cytokines.