To explore the effect of ligustrazine injection (LI) on serum levels of interleukin-4 (IL-4) and interferon-γ (IFN-γ) in patients with bronchial asthma and determine the mechanism of action of LI in preventing and treating asthma. Sixty-eight patients with mild or moderate bronchial asthma were assigned to two groups equally according to their sequence number

odd or even. The conventional treatment was administered to both groups

and LI was given to the treatment group by ultrasonic spray inhalation twice a day but not to the control group. The therapeutic course for all was 2 weeks. Further

30 healthy subjects who had no history of smoking were enrolled as the normal control group. The clinical condition scores

frequency of attacks and dosage of Terbutaline inhaled were scored and recorded on the first day of hospitalization (before treatment) and after treatment. At the same time

the indexes of lung function

including forced expiratory volume in one second (FEV1)

forced expiratory volume in one second to forced vital capacity ratio (FEV1%) and the peak expiratory flow (PEF) were determined before treatment. The levels of IL-4 and IFN-γ in peripheral blood were detected by ELISA before and after treatment

and compared with that of the healthy control group. After treatment

the clinical condition scores were found to be lower

indexes of lung function were elevated

but serum level of IL-4 and ratio of IL-4/IFN-γ were reduced in both groups

showing significant differences as compared to those before treatment (P<0.05). However

the changes in all the indexes were more significant in the treatment group than in the control group

also showing statistical significance (P<0.05). No significant difference was revealed when IFN-γ levels were compared before and after treatment in both groups

though a lowering trend could be seen

significant difference could not be found in the comparison of IFN-γ levels between groups after treatment (P>0.05). LI shows good clinical effect in treating bronchial asthma

and its mechanism might be related to the suppression of the synthesis of IL-4

thus leading to the inhibition of TH2 cell subset preponderant response and immune equilibrium regulation.