To discuss the effects of acacetin on lung injury in Mycoplasma pneumoniae pneumonia (MPP) mice and analyze the relationship between its mechanism and the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.

A MPP mouse model was constructed, and successfully modeled mice were stochastically divided into model group, low, medium and high dose acacetin experimental groups (acacetin-L, M, and H groups: 12.5, 25.0, and 50.0 mg·kg^-1 acacetin) and high-dose acacetin-H+JAK2 activator coumarin group (acacetin-H+coumarin 50 mg·kg^-1 acacetin-L and 2 mg·kg^-1 coumarin), each with 12 mice. Twelve normal healthy mice were intranasally instilled with an equal amount of physiological saline as the control group. Blood gas analyzer was used to detect arterial partial pressure of carbon dioxide (PaCO₂) and arterial partial pressure of oxygen (PaO₂) of mice, oxygen concentration analyzer was used to detect fraction of inspired oxygen (FiO₂), and the oxygenation index (OI) was calculated. Enzyme-linked immunosorbent assay (ELISA) was used to detect serum inflammatory factors. Biochemical method was used to detect oxidative stress indicators. The lung index and lung wet dry ratio were weighed and calculated. Hematoxylin-eosin (HE) staining was employed to evaluate the pathological lesions in lung tissue. Western blot assay was performed to detect the protein expression of JAK2/STAT3 signaling pathway-related molecules.

The OI value of the acacetin-L, -M, -H groups, control group, model group, and acacetin-H+coumamycin group were (274.63±30.02), (320.16±35.79), (374.55±39.88), (403.57±43.61), (220.31±26.78) and (241.03±29.14)mmHg, respectively; the IL-6 levels were (124.56±13.27), (87.61±9.23), (56.34±6.77), (36.50±4.15), (172.59±18.24) and (149.33±16.05)pg·mL^-1, respectively; the MDA contents were (4.06±0.45), (2.97±0.31), (1.93±0.22), (1.82±0.20), (5.31±0.58) and (4.69±0.49) nmol·mL^-1, respectively; the lung index was 1.31±0.15, 0.99±0.11, 0.57±0.07, 0.52±0.06, 1.78±0.19, and 1.54±0.17, respectively; the lung wet/dry weight ratio was (6.83±0.73)%, (5.61±0.58)%, (4.35±0.49)%, (4.10±0.45)%, (7.86±0.86)% and (7.33±0.81)%, respectively; the phosphorylated(p)-JAK2/JAK2 ratio were 0.71±0.08, 0.56±0.06, 0.43±0.05, 0.39±0.04, 0.86±0.09 and 0.79±0.08, respectively; the p-STAT3/STAT3 ratio were 0.67±0.07, 0.46±0.06, 0.30±0.04, 0.16±0.02, 0.83±0.09 and 0.74±0.08, respectively. There were statistically significant differences in the above indicators between the model group and the control group, between the acacetin-H group and the model group, and between the acacetin-H+coumarin group and the acacetin-H group (all P<0.05).

Acacetin can effectively improve lung injury in MPP mice, possibly by inhibiting the JAK2/STAT3 signaling pathway.