The Effect of Anion Inhalation in a Mouse Model of Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease

Oxidative/anti-oxidative stress unbalance is one of the mechanisms of chronic obstructive pulmonary disease (COPD). Anion has been shown to be effective to eliminate reactive oxygen species, yet it is unknown if inhalation of anion (IA) can be beneficial for COPD intervention.

COPD model mice were established by cigarette smoke (CS) exposure in combination with tracheal instillation of LPS, and treated with various dosages of IA for 120 days. Pulmonary function, inflammatory mediators, anti-oxidatives and collagen deposition level were measured to evaluate the therapeutic effects of IA in COPD model mice. The pathological morphology and structure of lung, liver, renal, spleen, heart, and brain were analyzed to assess the safety of IA.

IA improved COPD mice pulmonary function, reversed the decrease in SOD in blood serum and lung tissue, and increased the anti-oxidative stress protein NQO1 expression. IA could also decrease the collagen deposition and Smad2/3 phosphorylation in COPD mice lung. Additionally, IA did not affect the pathological structure and the index of major body organs.

This preclinical study demonstrated that IA is beneficial for COPD treatment, likely by increasing the anti-oxidative capacity and inhibiting Smad2/3 activation in lung tissue.