Abstract
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.
Keywords
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