János Bolyai Research Scholarship of the Hungarian Academy of Sciences(BO/00750/22/5)
New National Excellence Program of the Ministry for Innovation and Technology(ÚNKP-22-5-PTE-1740)
(UNKP-21-5-SZTE-577) Támogató: ÚNKP
(PD129114) Támogató: NKFIH
(FK143566) Támogató: NKFIH
(K135874) Támogató: NKFIH
(University of Szeged Open Access Fund (5892))
(KA-2022-29)
(TKP2021-EGA-16)
Various organosulfur compounds, such as dimethyl trisulfide (DMTS), display anti-inflammatory
properties. We aimed to examine the effects of DMTS on acute pancreatitis (AP) and
its mechanism of action in both in vivo and in vitro studies. AP was induced in FVB/n
mice or Wistar rats by caerulein, ethanol-palmitoleic acid, or L-ornithine-HCl. DMTS
treatments were administered subcutaneously. AP severity was assessed by pancreatic
histological scoring, pancreatic water content, and myeloperoxidase activity measurements.
The behaviour of animals was followed. Pancreatic heat shock protein 72 (HSP72) expression,
sulfide, and protein persulfidation were measured. In vitro acinar viability, intracellular
Ca 2+ concentration, and reactive oxygen species production were determined. DMTS
dose-dependently decreased the severity of AP. It declined the pancreatic infiltration
of leukocytes and cellular damage in mice. DMTS upregulated the HSP72 expression during
AP and elevated serum sulfide and low molecular weight persulfide levels. DMTS exhibited
cytoprotection against hydrogen peroxide and AP-inducing agents. It has antioxidant
properties and modulates physiological but not pathophysiological Ca 2+ signalling.
Generally, DMTS ameliorated AP severity and protected pancreatic acinar cells. Our
findings indicate that DMTS is a sulfur donor with anti-inflammatory and antioxidant
effects, and organosulfur compounds require further investigation into this potentially
lethal disease.