Electroacupuncture mitigates lung injury, increases endogenous antioxidant levels and modulates Nrf2 signaling in a rat model of chronic obstructive pulmonary disease.

BACKGROUND

Electroacupuncture (EA) has shown efficacy in the treatment of chronic obstructive pulmonary disease (COPD), but the underlying mechanism of action remains unclear. Oxidative stress is a main pathological process in COPD. This aim of this study was to explore the anti-oxidant effect of EA in a COPD rat model.

METHODS

Rats were divided into control, model, EA, sham acupuncture (SA) and N-acetylcysteine (NAC) groups. All rats except those in the control group were exposed to cigarette smoke combined with repeated bacterial infection to induce a COPD rat model. Rats in the EA group received EA at GV14 and bilateral BL13/BL23 for a further 8 weeks, while rats in SA group were given manual acupuncture at sites 5 mm from the traditional acupuncture point locations (without electrical stimulation) as a negative control. NAC (54 mg/kg/d) was used in the NAC group as a positive control. Lung function was assessed by whole body plethysmography, and tissue structure was assessed by histology. mRNA and protein levels of oxidative indicators and nuclear factor E2-related factor (Nrf2) signaling were measured by qPCR and immunohistochemistry or Western blotting, respectively.

RESULTS

After EA treatment, lung function and pathological features were improved. Total antioxidant capacity (T-AOC) and total superoxide dismutase (T-SOD) in serum, as well as SOD1 and heme oxygenase (HO)-1 in lung tissue, were increased, while markers of oxidative stress-lipid peroxidation (LPO) and malonaldehyde activity (MDA)-were decreased. Nrf2 protein in the nucleus of lung tissue, as well as HO-1 and γ-glutamylcysteine synthetase (γ-GCS) mRNA and protein, were improved. NAC, as an antioxidant, was better than EA at increasing the expression of HO-1 protein and γ-GCS mRNA.

CONCLUSIONS

EA was beneficial for the treatment of COPD in this rat model and exerted antioxidant effects via mechanisms potentially related to Nrf2 signaling.