Wednesday, 14 October 2015
Hall D1 Foyer (Floor 3) (Coex Convention Center)
Background: S-nitrosoglutathione reductase (GSNOR) is an important regulator for S-nitrosoglutathione (GSNO), the main source of bioavailable NO, and protects cells from nitrosative stress. We hypothesized that aerosol delivery of GSNO could reduce bronchoconstriction and pulmonary inflammation in a mouse model of asthma.
Methods: To evaluate whether GSNO could ameliorate AHR and inflammation, we compared AHR and inflammation in the 6-week-old female BALB/c mice treated with 0.3 cc aerosolized 0-10 mM GSNO.
Results: GSNO inhalation significantly decreased airway hyperresponsiveness with the increasing GSNO dose up to 0.03 ng/ml. But increasing the dose of GSNO more over than 0.03 ng/ml, there was absence of bronchoprotection or even aggravation of bronchocontriction.
Conclusions: These results suggested that GSNO may be an important factor to control airway hyperresponiveness, and there might be a concentration threshold for an effective action of GSNO.