Objective: To investigate the effect of Yulangsan (YLS) extracts on acute lung injury in rats. Method: The Wistar rats were randomly divided into control group

model group

dexamethasone group(3 mg·kg-1)

high and low dose groups of total YLS water extract (TYLS) (60

30 g·kg-1)and flavonoids extracted from the roots of YLS(FYLS)(0.1

0.05 g·kg-1). The animals were intragastrically treated with drugs for 7 days.The ALI model was set up by intraabdominal injection of 20% yeast suspension 5 mL·kg-1

two time 30 minutes after the last medication.The lung wet/dry weight ratio(W/D) and the activity of myeloperoxidase(MPO) in the lung tissues were determined to assess lung injury. The expression of nuclear factor κB(NF-κB) p65 was analyzed by immunohistochemistry. The content of interleurin-1β(IL-1β)in the lung tissue was detected by ELISA. Meanwhile

the pathological change of lung was also observed by HE dying. Result: As compared with the control group

the lung W/D

MPO activity

IL-1β content and expression of NF-κB p65 were higher in the model group(P<0.01). HE dying showed inflammatory changes in lung in the model group. In TYLS high-and low-dose groups and FYLS high dose group

the lung W/D was (4.31±0.15)

(4.72±0.35)

(4.74±0.23) respectively

was significantly lower compared with model group(P<0.05

P<0.01). The MPO activity was (1.000± 0.304)

(0.956±0.139 )U·g-1

IL-1β content was(265.58±47.05)

(222.31± 53.99)ng·L-1

NF-κB p65 expression level was(51.00±8.62)%

(48.88±11.80)%

in the high dose group of TYLS and FYLS respectively. The MPO activity and IL-1β content and NF-κB p65 expression level in lung were significantly reduced compared with model group(P<0.05

P<0.01).On the other hand

histopathological examination confirmed that the degree of lung injury in TYLS and FYLS groups was lessened. And high-dose groups showed the best effect. Conclusion: Preliminary administration of YLS extracts can alleviate the degree of pulmonary edema and pulmonary inflammation. The effects may be related to inhibiting the production of IL-1β by interfering the NF-κB path.