1065 Protection from airway bronchoconstriction by gsno

Wednesday, 14 October 2015
Hall D1 Foyer (Floor 3) (Coex Convention Center)

Jin-Young Lee, MD, PhD , Health Promotion Center, Samsung Medical Center, Seoul, South Korea

Yun-Jin Jeung, MD , Clean Medicine Allergy Clinic, Seoul, South Korea

Mi-Jung Oh, MD, PhD , Bundang Jesaeng Hospital, BUNDANG, South Korea

Young Hee Lim, MD, PhD , Sarang General Hospital, Ansan, South Korea

Kyoung Won Ha, MD , Seoul Samsung Medical Clinic, Incheon, South Korea

Mi-Jin Jang , Samsung Biomedical Research Institute, Seoul, South Korea

Jae-Won Paeng , Samsung Biomedical Research Institute, Seoul, South Korea

Sehyo Yune, MD , Department of Medicine, Samsung Medical Center, Seoul, South Korea

Byung-Jae Lee, MD, PhD , Samsung Medical Center, Seoul, South Korea

Dong-Chull Choi, MD, PhD , Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea

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.