Abstract: BACKGROUND: Studies have shown that mitochondrial apoptosis of alveolar epithelial cells plays an important role in the pathogenesis of pulmonary fibrosis, and Feibi prescription can attenuate pulmonary fibrosis and inhibit the transformation of extracellular mechanisms in mice with pulmonary fibrosis.  
OBJECTIVE: To investigate the mechanism of Feibi prescription on mitochondrial apoptpsis of alveolar epithelial cells in bleomycin induced pulmonary fibrosis mice. 
METHODS: Forty male C57BL/6 mice were randomly divided into blank control group, model group, pirfenidone group, and Feibi prescription group. There were 10 mice in each group. Except for the blank control group, the other three groups were intraperitoneally injected with bleomycin (7.5 mg/kg per day) for 10 continuous days to establish the model of pulmonary fibrosis. On day 1 after modeling, the mice in corresponding drug groups were intragastrically administered with pirfenidone (51.43 mg/kg per day) or Feibi prescription (12.86 mg/kg per day). Drug administration lasted for 28 days. Then, morphological changes of lung tissue in mice were observed by hematoxylin-eosin staining and Masson staining. The levels of interleukin-1, interleukin-6, interleukin-17, and interleukin-37 in the serum were detected by ELISA, and the expression of Bax, Bcl-2, Beclin-1, and Caspase3 in the lung tissue was detected by western blot assay. 
RESULTS AND CONCLUSION: Morphological observation of lung tissue showed that in the model group, the alveolar septum and alveolar lumen were infiltrated with a large number of inflammatory cells, and there were large clusters of fibrous foci; in the pirfenidone group, alveolar septa were thickened, with a small infiltration of inflammatory cells and the appearance of pulmonary fibrous foci; in the Feibi prescription group, the alveolar structure was widened, with a small amount of inflammatory cell infiltration, and the alveolar structure was almost not obviously damaged, with a small number of lung fibrous foci. Compared with the blank control group, the mass concentrations of interleukin-1, interleukin-6, interleukin-17, and interleukin-37 were significantly higher in the model group (P < 0.01), while the levels were significantly lower in the two drug groups than the model group (P < 0.01). Moreover, the mass concentrations of interleukin-1, interleukin-6, interleukin-17, and interleukin-37 in the Feibi prescription group were lower than those in the pirfenidone group. Compared with the blank control group, the expression of Bax and Caspase3 proteins in the lung tissue of mice was significantly higher in the model group, while the expression of Bax and Caspase3 proteins was significantly lower in the two drug groups than the model group. Compared with the blank control group, the expression of Bcl-2 and Beclin-1 proteins in the lung tissue of mice was significantly lower in the model group, while the expression of Bcl-2 and Beclin-1 proteins was significantly higher in the two drug groups than the model group. To conclude, Feibi prescription can reduce pulmonary fibrosis and its mechanism may be related to the downregulation of interleukin-1, interleukin-6, interleukin-17, and interleukin-37 levels. This prescription can also reduce the apoptosis of alveolar epithelial cells by regulating mitochondrial apoptosis-related proteins, Bax, Bcl-2, Beclin-1 and Caspase3.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Feibi prescription, pulmonary fibrosis, mitochondrion, bleomycin, C57BL/6 mouse