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

Abstract

To explore the potential biological mechanism of chronic obstructive pulmonary disease (COPD) qi deficiency syndrome, we used the integrated pharmacology network computing platform and carried out experimental verification. Using an integrated pharmacology strategy to analyze the potential biological targets of COPD qi deficiency syndrome. 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. According to the integrated pharmacological results, it was found that the locations of cell components related to COPD qi deficiency syndrome were mainly mitochondria. Electron microscopy results using lung tissue showed that mitochondria in the lipopolysaccharide (LPS group) and pulmonary instillation of LPS combined with cigarette smoke (LPS+CS group) were swollen, deformed, and fragmented, with disappearing or broken crista. 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 12 th week ( P < .05). At the 12 th week, the expression of dynamin-related protein 1 (DRP1) and mitofusin 1 (MFN1) protein was significantly difference than that of the control group ( P < .05). At the 10 th and 14 th weeks, changes in fission and fusion proteins in mitochondria of the lung and skeletal muscle were further detected. There was also a significant difference in the expression between the two groups compared to that in the control group at the 10 th week and 14 th week ( P < .05). 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.