To investigate the mechanism of action of Bufei Decoction（补肺汤）in intervening chronic obstructive pulmonary disease（COPD）lung Qi deficiency by modulating the levels of mitochondrial autophagy mediated by phosphatase and tensin homolog-induced putative kinase protein 1（PINK1）/RBR domain E3 ubiquitin protein ligase（Parkin）signaling path-way.

The rats were randomly divided into the control group and the modeling group, and a rat model of COPD lung Qi deficiency was created by using passive smoke inhalation combined with intra-airway lipopolysaccharide drip. At the end of modeling, the rats in the modeling group were randomly divided into the model group, Bufei Decoction medium-dose group, Bufei Decoction high-dose group and 3-methyladenine（3-MA）group. The Bufei Decoction medium - and high-dose groups were given Bufei Decoction drug solution by gavage（7.29, 14.58 g·kg^-1）, and 3-MA group was given 3-MA（15 mg·kg^-1）by intraperitoneal injection, and each group was intervened with the drug once daily for 28 d consecutively. Hematoxylineosin（HE）staining was used to observe the pathological changes in lung tissues. The transmission electron microscopy was used to observe ultrastructural changes in alveolar type Ⅱ epithelial cells in lung tissues. The immunohistochemistry（IHC）method was used to detect the positive expressions of PINK1, Parkin, autophagy receptor protein P62（sequestosome 1, P62/SQSTM1）and microtubule-associated protein 1 light chain 3（LC3）proteins in lung tissues and protein immunoblotting（Western blot）to detect the expressions of PINK1 in mitochondria in lung tissues, Parkin, P62, LC3Ⅱ/LC3I protein expression in mitochondria of lung tissues. Flow cytometry detected the changes of mitochondrial membrane potential in lung tissues. The reactive oxygen species fluorescent probe dichloro-dihydro-fluorescein diacetate（DCFH-DA）and mitochondrial superoxide（MitoSOX）red fluorescent probe were used to determine the levels of reactive oxygen species（ROS）and mitochondrial reactive oxygen species（mtROS）in lung tissues by flow cytometry, respectively. Western blot detected the expressions of nuclear factor-κB P65（NF-κB P65）and phosphorylation of nuclear factor-κB P65（p-NF-κB P65）proteins in lung tissues.

Compared with that in the control group, the lung tissue damage in the model group was severe. Compared with that in the model group, the pathological damages in the Bufei Decoction medium - and high-dose groups and 3-MA group were improved to different degrees. Compared with those of the control group, the lung tissue of the model group showed severe damage to alveolar type Ⅱ epithelial cells and their mitochondrial structure, with a decrease in mitochondria and an increase in autophagic vesicles. Compared with those of the model group, the alveolar type Ⅱ epithelial cells and their mitochondrial structure of the model group showed a lesser degree of damage in the Bufei Decoction medium - and high-dose groups and the 3-MA group, with a relatively higher increase in mitochondria and a decrease in autophagic vesicles. Compared with those in the control group, the protein expressions of PINK1, Parkin, LC3 and LC3Ⅱ/LC3I were up-regulated（P<0.01）and the protein expression of P62 was down-regulated（P<0.01）in the lung tissues and mitochondria of lung tissue in the model group. Compared with those in the model group, the protein expressions of PINK1, Parkin and LC3Ⅱ/LC3I were up-regulated（P<0.01）and the protein expression of P62 was down-regulated（P<0.01）in the lung tissues and mitochondria of lung tissue in the Bufei Decoction medium - and high-dose groups and 3-MA group. The protein expressions of PINK1, Parkin, LC3 and LC3Ⅱ/LC3I were down-regulated（P<0.05, P<0.01）and P62 protein expression was up-regulated（P<0.01）. Compared with those in the control group, the mitochondrial membrane potential of lung tissues in the model group was decreased（P<0.01）, the levels of ROS and mtROS were up-regulated（P<0.01）, the difference in the expression of NF-κB P65 protein was not statistically significant, and the expression of p-NF-κB P65 protein was up-regulated（P<0.01）. Compared with those of the model group, the mitochondrial membrane potential in the lung tissues of the Bufei Decoction medium - and high-dose groups and the 3-MA group were elevated（P<0.01）, the levels of ROS and mtROS were down-regulated（P<0.01）, and the differences in the expression of NF-κB P65 proteins were not statistically significant, and the expression of p-NF-κB P65 protein was down-regulated（P<0.01）.

Bufei Decoction inhibited lung tissue ROS levels and the activation of NF-κB P65, thereby attenuating the oxidative damage and inflammatory responses in the lung of COPD lung Qi deficiency, and its mechanism of action may be related to the inhibition of the level of mitochondrial autophagy mediated by the PINK1/Parkin signaling pathway.