Involvement of endogenous hydrogen sulfide in cigarette smoke-induced changes in airway responsiveness and inflammation of rat lung.

摘要: Hydrogen sulfide (H₂S), recently considered the third endogenous gaseous transmitter, may have an important role in systemic inflammation. We investigated whether H₂S be a crucial mediator airway responsiveness and inflammation rat model of chronic exposure to cigarette smoke (CS). Rats randomly divided into control CS-exposed groups were treated with or without sodium hydrosulfide (NaHS, donor H₂S) propargylglycine (PPG, inhibitor cystathionine-γ-lyase [CSE], H₂S-synthesizing enzyme) for 4-month exposure. Serum level CSE protein expression lung tissue higher, by 2.04- 2.33-fold, respectively, rats than controls (P<0.05). Exogenous administration NaHS alleviated reactivity induced acetylcholine (Ach) potassium chloride (KCl) 17.4% 13.8%, decreased pathology score 32.7%, inhibited IL-8 TNF- α concentrations 34.2% 31.4%, as compared (all P<0.05). However, blocking PPG increased Ach KCl, 24.1% 24.5%, aggravated score, 44.8%, P<0.01). Incubation vitro NaHS, 1-3 mmol/L, relaxed tracheal smooth muscle precontracted KCl. NaHS-induced relaxation was not blocked glibenclamide (10⁻⁴ mol/L), L-NAME ODQ (1 μmol/L) denudation epithelium. Endogenous protective anti-inflammation bronchodilation CS-induced pulmonary injury.