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. 2017 Oct;57(4):403–410. doi: 10.1165/rcmb.2017-0114TR

Table 1.

Summary of H2S Treatment in Animal Models of Lung Diseases

Disease Model H2S Donor(s) Findings References
Asthma (mouse, rat) NaHS ↓ Airway hyperresponsiveness (32)
↓ Inflammation (33)
↓ Oxidative stress (53)
↓ Mast cell degranulation (54)
↓ Fibroblast recruitment and proliferation
↓ Pathology
↑ Lung function
COPD (mouse, rat) NaHS ↓ Pathology (39)
↓ Inflammation (40)
↓ Airway hyperresponsiveness
↑ Lung function
↓ Oxidative stress
↓ Apoptosis
Pulmonary fibrosis (mouse, rat) NaHS ↓ Pathology (56)
↓ Oxidative stress (57)
↓ Inflammation (58)
↓ Fibrosis  
Allergic rhinitis (guinea pig) NaHS ↓ Clinical disease (44)
↓ Inflammation
Acute lung injury (mouse, rat) DATS ↓ Inflammation (61)
GYY4137 ↓ Oxidative stress (65)
DTT ↓ Clinical disease (73)
RSV infection (mouse) GYY4137 ↓ Clinical disease (50)
↓ Airway hyperresponsiveness
↓ Viral replication
↓ Inflammation

Definition of abbreviations: COPD, chronic obstructive pulmonary disease; DATS, diallyl trisulfide; GYY4137, phosphorodithioate-based donor; DTT, 1,2-dithiole-3-thiones; NaHS, sodium hydrosulfide; RSV, respiratory syncytial virus.