Exploring the biological mechanism of qi deficiency syndrome with chronic obstructive pulmonary disease (COPD) based on integrated pharmacology

Abstract Objective Using the integrated pharmacology network computing platform, we analyzed the potential biological mechanism of chronic obstructive pulmonary disease (COPD)-Qi deficiency syndrome and carried out experimental verification. Methods By using an integrated pharmacology strategy, a multi-level network of the \"COPD-Qi deficiency syndrome-Core target-Key pathway\" was constructed to analyze the potential biological targets of COPD-Qi deficiency syndrome. The COPD rat model was established through two methods comprising pulmonary instillation of lipopolysaccharide (LPS group) and pulmonary instillation of LPS combined with cigarette smoke (LPS + CS group). Based on the established Qi deficiency syndrome rat model of COPD, the biological targets of lung and skeletal muscle were detected by electron microscopy, adenosine triphosphate (ATP) content assays, and western blotting. Results According to the integrated pharmacological results, it was found that the locations of cell components related to COPD-Qi deficiency syndrome were mainly mitochondria, the mitochondrial inner membrane, and mitochondrial respiratory chain complex II, among others. Electron microscopy results using lung tissue showed that mitochondria in the LPS and LPS + CS groups were swollen, deformed, and fragmented, with disappearing or broken crista, and the morphological changes in mitochondria in LPS + CS group were more prominent than those in the LPS group at the 12th week. Results also showed that the total content of ATP in the lung and skeletal muscle of both groups was significantly lower than that in the control group at the 12th week (P  Conclusion These findings suggest that the changes in mitochondrial morphology and ATP content and the unbalanced expression of DRP1 and MFN1 might be the key mechanisms underlying Qi deficiency syndrome in rats with COPD.