Effects of hydrogen sulfide on inflammation in caerulein-induced acute pancreatitis.

J Inflamm (Lond)

Cardiovascular Biology Research Group, Department of Pharmacology, Yong Loo Lin School of Medicine, CRC MD11, National University of Singapore 117597, Singapore, Singapore.

Published: December 2009

Background: Hydrogen sulfide (H(2)S), a gaseous mediator plays an important role in a wide range of physiological and pathological processes. H(2)S has been extensively studied for its various roles in cardiovascular and neurological disorders. However, the role of H(2)S in inflammation is still controversial. The current study was aimed to investigate the therapeutic potential of sodium hydrosulfide (NaHS), an H(2)S donor in in vivo model of acute pancreatitis in mice.

Methods: Acute pancreatitis was induced in mice by hourly caerulein injections (50 mug/kg) for 10 hours. Mice were treated with different dosages of NaHS (5 mg/kg, 10 mg/kg or 15 mg/kg) or with vehicle, distilled water (DW). NaHS or DW was administered 1 h before induction of pancreatitis. Mice were sacrificed 1 h after the last caerulein injection. Blood, pancreas and lung tissues were collected and were processed to measure the plasma amylase, myeloperoxidase (MPO) activities in pancreas and lung and chemokines and adhesion molecules in pancreas and lung.

Results: It was revealed that significant reduction of inflammation, both in pancreas and lung was associated with NaHS 10 mg/kg. Further the anti-inflammatory effects of NaHS 10 mg/kg were associated with reduction of pancreatic and pulmonary inflammatory chemokines and adhesion molecules. NaHS 5 mg/kg did not cause significant improvement on inflammation in pancreas and associated lung injury and NaHS 15 mg/kg did not further enhance the beneficial effects seen with NaHS 10 mg/kg.

Conclusion: In conclusion, these data provide evidence for anti-inflammatory effects of H(2)S based on its dosage used.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2804662PMC
http://dx.doi.org/10.1186/1476-9255-6-35DOI Listing

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