Effects of S-Propargyl-Cysteine (SPRC) in Caerulein-Induced Acute Pancreatitis in Mice
Open Access
- 1 March 2012
- journal article
- research article
- Published by Public Library of Science (PLoS) in PLOS ONE
- Vol. 7 (3), e32574
- https://doi.org/10.1371/journal.pone.0032574
Abstract
Hydrogen sulfide (H2S), a novel gaseous messenger, is synthesized endogenously from L-cysteine by two pyridoxal-5′-phosphate-dependent enzymes, cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE). S-propargyl-cysteine (SPRC) is a slow H2S releasing drug that provides cysteine, a substrate of CSE. The present study was aimed to investigate the effects of SPRC in an in vivo model of acute pancreatitis (AP) in mice. AP was induced in mice by hourly caerulein injections (50 µg/kg) for 10 hours. Mice were treated with SPRC (10 mg/kg) or vehicle (distilled water). SPRC was administered either 12 h before or 3 h before the induction of pancreatitis. Mice were sacrificed 1 h after the last caerulein injection. Blood, pancreas and lung tissues were collected and processed to measure the plasma amylase, plasma H2S, myeloperoxidase (MPO) activities and cytokine levels in pancreas and lung. The results revealed that significant reduction of inflammation, both in pancreas and lung was associated with SPRC given 3 h prior to the induction of AP. Furthermore, the beneficial effects of SPRC were associated with reduction of pancreatic and pulmonary pro-inflammatory cytokines and increase of anti-inflammatory cytokine. SPRC administered 12 h before AP induction did not cause significant improvement in pancreatic and lung inflammation. Plasma H2S concentration showed significant difference in H2S levels between control, vehicle and SPRC (administered 3 h before AP) treatment groups. In conclusion, these data provide evidence for protective effects of SPRC in AP possibly by virtue of its slow release of endogenous H2S.This publication has 37 references indexed in Scilit:
- Hydrogen Sulfide Improves Neutrophil Migration and Survival in Sepsis via K+ATPChannel ActivationAmerican Journal of Respiratory and Critical Care Medicine, 2010
- Hydrogen sulfide therapy attenuates the inflammatory response in a porcine model of myocardial ischemia/reperfusion injuryThe Journal of Thoracic and Cardiovascular Surgery, 2009
- Hydrogen Sulfide-Induced Hypometabolism Prevents Renal Ischemia/Reperfusion InjuryJournal of the American Society of Nephrology, 2009
- Hydrogen sulphide and its therapeutic potentialNature Reviews Drug Discovery, 2007
- Hydrogen sulfide (H2S) - the third gas of interest for pharmacologists.2007
- Inhibition of endogenous hydrogen sulfide formation reduces the organ injury caused by endotoxemiaBritish Journal of Pharmacology, 2005
- Hydrogen sulphide is a mediator of carrageenan‐induced hindpaw oedema in the ratBritish Journal of Pharmacology, 2005
- Hydrogen sulfide is a novel mediator of lipopolysaccharide‐induced inflammation in the mouseThe FASEB Journal, 2005
- Role of hydrogen sulfide in acute pancreatitis and associated lung injuryThe FASEB Journal, 2005
- Role of hydrogen sulphide in haemorrhagic shock in the rat: protective effect of inhibitors of hydrogen sulphide biosynthesisBritish Journal of Pharmacology, 2004