Codonopsis Radix inhibits the inflammatory response and oxidative stress in Chronic Obstructive Pulmonary Disease mice through regulation of the Nrf2/NF-κB signaling pathway.

Abstract

INTRODUCTION Chronic Obstructive Pulmonary Disease (COPD) is a non-specific chronic inflammatory lung disease with no known cure. Codonopsis Radix(CR) has been shown to exhibit anti-inflammatory and antioxidant effects. Therefore, this study aimed to investigate the potential anti-inflammatory effects of different CR variety on COPD mice. METHODS 60 male specified pathogen free (SPF)-grade C57BL/6J mice were randomly divided into 6 groups, 10 mice in each group. The COPD mice model was induced by cigarette smoke extract (CSE) combined with lipopolysaccharide (LPS), and the mice in each group were given corresponding drugs. Lung function was assessed in all mice. Lung tissues were stained with hematoxylin-eosin (HE), Masson, and periodic acid shiff (PAS) stains, and serum levels of interleukin (IL)-8 and tumor necrosis factor (TNF)-α were detected using an enzyme-linked immunosorbent assay (ELISA). Further, serum and lung tissue levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by colorimetric assay. Network pharmacology and molecular docking was used to predict signalling pathways, which were validated by western blot analysis. RESULTS Compared with the COPD group, the mice in each dosing group of CR exhibited significant reductions in serum IL-8 and TNF-α levels, serum and lung tissue MDA levels, and pathological lung tissue damage, alongside elevations in lung function and SOD levels (P<0.01). Western blot analysis also indicated significant down-regulation of p-p65/p65 and p-IκB-α/IκB-α protein expression, alongside significant up-regulation of Nrf2 protein expression in the lung tissues of mice treated with CR (P<0.01). CONCLUSION In summary, CR effectively enhances lung function, minimizes lung tissue damage, and inhibits inflammation and oxidative stress in mice with COPD. Additionally, these findings suggest that inhibition of the Nrf2/NF-κB axis may be a key mechanism of action of CR in the alleviation of COPD.