The naringin's influence on the protein expressions in the lung tissues of cigarette smoke induced acute lung inflammation in mice was examined by iTRAQ technology. Twenty Balb/c mice were randomly divided into the model group and the naringin group with ten mice in each group. Naringin was administered by gavage at a dose of 60 mg（·kg

-1

·d

-1

） before smoke treatment

while mice in model group were given normal saline. All mice were sacrificed 16 h after the last smoke treatment. The lung tissues were collected and analyzed by iTRAQ technology. Differentially expressed proteins were screened through identification and quantification analysis. As a result

a total of 3 528 proteins were identified

of which 64 proteins were differentially expressed after administration of naringin

including 29 up-regulated and 35 down-regulated proteins. Bioinformatics analysis indicated that these differentially expressed proteins were mainly associated with the release of inflammatory mediator nitric oxide and the metabolism of pro-oxidant agent homocysteine. These may provide an important contribution to naringin's effects on the protection of lung tissue injury caused by inflammation and promotion of inflammation resolution. Arg1

Bhmt and Dnmt may play important roles in the therapeutic effects of naringin on the lung inflammation diseases. The present study could provide a useful basis for the mechanism study of naringin.