Objective To discuss the potential mechanism of Qingjin Huatan Granule（ QJHTG）（ 清金化痰颗粒） in treating acute exacerbation of chronic obstructive pulmonary disease（ AECOPD） with phlegm-heat stagnating in lung. Methods A total of 40 Sprague Dawley rats were randomized into blank group

model group

western medicine group and the low

high dose QJHTG groups

with 8 rats in each group. The rat model of phlegm-heat stagnating in lung of AECOPD was established by smoking and dripping the LPS into the trachea except those in the blank group. After modeling

the western medicine group was intragastrical administration 0. 0315 g/（ kg·d） of roxithromycin（ ROX）. The low

high dose QJHTG groups were respectively intragastrical administration 9. 4 g/（ kg·d）

and37. 6 g/（ kg · d） of QJHTG. The blank group and the model group were respectively intragastrical administration10 ml/（ kg·d） of normal saline. After 2 weeks’ drug administration

the inflammatory mediators contents of interleukin-1β（ IL-1β）

tumor necrosis factor-α（ TNF-α） in bronchoalveolar lavage fluid（ BALF） in each group were observed

and the expression of Janus kinase 2（ JAK2） and suppressors-of-cytokine-signaling 3（ SOCS3） mRNA in lung tissues was detected. The phosphorylation signal transducer and activator of transcription 1（ p-STAT1）

phosphorylation signal transducer and activator of transcription 3（ p-STAT3）

JAK2

p-JAK2

SOCS3 protein expression were detected by Western Blot. Results After drug administration

compared with the model group

the inflammatory mediators contents of IL-1β

TNF-α in BALF in the QJHTG groups were significantly decreased

and JAK2 mRNA and protein expression

p-STAT1

p-STAT3

p-JAK2 protein expression decreased obviously in the lung tissues. SOCS3 mRNA and protein expression significantly increased in the lung tissues（ P < 0. 05 or P < 0. 01）. The effects of high dose QJHTG group and western medicine group was similar（ P > 0. 05）. The effects of low dose QJHTG group were lower than that of high dose QJHTG group and Western medicine group（ P < 0. 05 or P < 0. 01）.Conclusion One of the mechanisms for QJHTG treatment phlegm-heat stagnating in the lung of AECOPD may be by down-regulated the expression of p-STAT1

p-STAT3

JAK2

p-JAK2 and up-regulated the expression of SOCS3

consequently inhibiting the inflammatory response of AECOPD and alleviating the lung tissue injury. The high dose shows better effects.