Objective: To explore the effect of Qingjin Huatan granule (QJHTG) on regulation of transcriptional activator and signal transducer STAT1 and STAT3 in lung tissues of rat models with acute exacerbation of chronic obstructive pulmonary disease (COPD) (phlegm-heat stagnating in lung). Method: COPD rat models with phlegm-heat stagnating in lung were established by smoking and intratracheal injection of LPS (except normal group). The rats were randomly divided into normal group

model group

roxithromycin (ROX) group (0.031 5 g·kg-1)

QJHTG low dose group and high dose group (9.40

37.6 g·kg-1)

n=8 in each group. The medicines were given once a day by ig administration for 2 weeks. General activities and pathological change features were observed in all groups. The lung function indexes of rats were measured by using lung function tester:forced expiratory volume in 0.3 second (FEV0.3)

force vital capacity (FVC)

FEV0.3/FVC and vital capacity (VC). The mRNA expression levels of interleukin-6 (IL-6)

STAT1 and STAT3 in lung tissues were determined by Real-time PCR method and the protein expression levels of IL-6

STAT1 and STAT3 in lung tissues were determined by immunohistochemical method. Result: As compared with the normal group

the mRNA expression levels of IL-6

STAT1 and STAT3 in lung tissues of model group were significantly increased (P<0.01). As compared with the model group

the mRNA expression levels of IL-6

STAT1 and STAT3 in lung tissues were significantly decreased in ROX group

QJHTG low and high dose groups (P<0.01)

and the decrease was more obvious in ROX group and QJHTG high dose group

with no significant difference between these two groups. The average optical density of IL-6

STAT1 and STAT3 protein expression in the model group was significantly higher than that in the normal group (P<0.01); the pulmonary function parameters of rats in model group

including FEV0.3

FVC

FEV0.3/FVC and VC were lower than those in normal group (P<0.01). As compared with the model group

FEV0.3

FVC

and VC values were increased in various treatment groups (P < 0.01

P < 0.05); the average optical density of IL-6

STAT1 and STAT3 was significantly decreased in ROX group

QJHTG low and high dose groups (P<0.01)

and the decrease was more obvious in ROX group and QJHTG high dose group

with no statistical differences between these two groups. Conclusion: QJHTG can inhibit the increase of IL-6

reduce airway inflammation

and inhibit COPD acute attack and exacerbation by down-regulating excessive expression and sustained activation of STAT1 and STAT3 in the JAK/STAT signaling pathway.