The effect of hydrogen sulfide, a gas signaling molecule, on severe acute pancreatitis induced lung injury in rats

Objective To investigate the effect of hydrogen sulfide (H2S),a gas signaling molecule,on severe acute pancreatitis (SAP) induced lung injury in rats.Methods A total of 60 Wistar rats were randomized into 4 groups of 15,including a sham group,SAP group,sodium hydrosulfide (NaHS) group,and DL-propargylglycine (PAG) group.The rats received an intraperitoneal injection of NaHS and PAG 1 hour after operation in the NaHS and PAG group respectively.The remaining living animals in each group were sacrificed 24 hours after SAP models were developed to determine the pulmonary cystathionine-γ-1yase (CSE) activity and mRNA expression.The myeloperoxidase (MPO),phospholipase A2 (PLA2),and nuclear factor-κB (NF-κB)activity were evaluated.The wetdry weight ratio,as well as the levels of intercellular cell adhesion molecule-1 (ICAM-1),substance P,maleic dialdehyde (MDA),tumor necrosis factor-α (TNF-α),and interleukin-1β (IL-1β) were determined.The pathologic changes in the pancreas and lung were analyzed,and the serum contents of H2S,TNF-α,and IL-1β was found.Results Compared with the SAP group,every index was significantly increased in the NaHS group (P＜0.05) and obviously lowered in the PAG group (P＜0.05).Conclusion In severe acute pancreatitis,endogenous H2S levels are obviously increased leading to secondary lung injury.Therefore,inhibition of systemic and tissular H2 S production may protect against SAP-induced lung injury to some extent.The mechanism of action may be related to suppressing overinflammation,abating oxidative stress,and ameliorating microcirculatory disorder. Key words: Acute necrotizing pancreatitis;  Hydrogen sulfide;  Lung injury