Published online Apr 21, 2015. doi: 10.3748/wjg.v21.i15.4555
Peer-review started: July 31, 2014
First decision: August 27, 2014
Revised: September 20, 2014
Accepted: December 5, 2014
Article in press: December 8, 2014
Published online: April 21, 2015
AIM: To study the effect of hydrogen sulfide (H2S) on severe acute pancreatitis (SAP) in a rat model.
METHODS: Sprague-Dawley (SD) rats were administered an intraperitoneal injection of saline containing 20% L-Arg (250 mg/100 g) hourly for over 2 h to induce SAP. The rats were treated with DL-propargylglycine (PAG, 50 mg/kg) or different dosages of NaHS (5 mg/kg, 10 mg/kg, 20 mg/kg or 100 mg/kg). PAG or NaHS was administered 1 h before induction of pancreatitis. Rats were sacrificed 24 h after the last L-Arg injection. Blood and pancreas tissues were collected.
RESULTS: The H2S and cystathionine-γ-lyase mRNA levels in SAP rats were significantly lower than those in the control group, and treatment with PAG further reduced the H2S level. Nevertheless, H2S was significantly increased after NaHS administration compared with the SAP group, and the degree of upregulation was associated with the NaHS dosage. NaHS reduced the levels of plasma amylase, interleukin-6 and myeloperoxidase in pancreatic tissue. NaHS suppressed the degradation of IκBα and the activity of nuclear factor-κB, as well as the phosphorylation of PI3K/AKT.
CONCLUSION: H2S plays an anti-inflammatory role in SAP in vivo.
Core tip: In this research, we provide wide-ranging dosages of exogenous H2S (NaHS), from 5 mg/kg to 100 mg/kg, to study the role of H2S in severe acute pancreatitis (SAP) in vivo, and finally found that the level of H2S was reduced in rat SAP models, suggesting that H2S donor NaHS reduced the inflammatory indices of SAP, by inhibiting PI3K/AKT phosphorylation and down-regulating IκBα degradation and nuclear factor-κB activity.