Chitosan oligosaccharide (100 kDa and 90% deacetylation) prevented inflammation, oxidative stress and apoptosis in the lung tissues of blast injury-induced mice by diminishing protein expression of p38 and ADMA (an inhibitor of endogenous nitric oxide synthase that positively correlated with hypertension) and recovering dimethylarginine dimethylaminohydrolase 1 (DDAH1), a hydrolase of ADMA [85]. The gene discussed is DDAH1; the disease is Hypertension.