Abstract: Objective：To observe the effect of Qingzao Jiufei decoction (QJD) and its decomposable agent on the toll-like receptors(TLR) 2/myeloid differentiation primary response gene 88 (MyD88) / (NF-κB) signal pathway in MP infected mice，and to explore its mechanism of action of resistance to MP.Methods：Totally 144 BALB/c mice, about 20 g in weight, were randomly divided into normal group(A),model group(B),QJD group(C),QJD decomposable agentⅠgroup(D),QJD decomposable agent Ⅱ group(E) and azithromycin group(F),with 24 mice in each group. Each treatment group was made into MP infection model and the corresponding group was given corresponding drugs by intragastric administration after modeling. The serum and the lung tissues were detected after 3,7,10 and 14 days of MP infection. HE staining was used to observe the pathological change of lung tissues, qPCR was used to detect the changes of TLR-2 mRNA in lung tissues, ELISA was used to detect the expressions of MyD88 and TNF-α in serum, and Western blot was used to detect the expression levels of NF-κB in lung tissues.Results：The interstitial inflammatory changes of lung occurred 3d after MP infection，which were most significant on the 7d，and then gradually became less and less significant. Pulmonary inflammation in each treatment group was improved, especially in Group C and Group F on the 10d and 14d. The expression level of TLR-2 and NF-κB in the lung tissue of mice after MP infection increased, and the content of MyD88 and TNF-α in serum was also increased(P<0.05).The peak time of each indicator was different with NF-κB appearing earliest (3rd day),TLR-2 and TNF-α peaking on the 7th day, while MyD88 was relatively late，peaking on the 10th day. On the 7th day in Group C(P＜0.05),the expression level of TLR-2 and NF-κB in lung tissue decreased, and the content of MyD88 and TNF-α in serum was also decreased. Group D also played a similar role to Group C on the 10th day and 14th days, but weaker than Group C (P＞0.05); in Group E on the 14th day TLR-2 mRNA expression slightly increased.Conclusion：The mechanism of QJD against MP infection is associated with reducing the release of proinflammatory factors and regulating the conduction of TLR-2/NF-κB signaling pathway，in which the decomposition agent Ⅰ plays a major role.

Key words: Mycoplasma pneumoniae, Qingzao Jiufei decoction, TLR-2/NF-κB signal pathway, Mice