Effects of S-propargyl-cysteine (SPRC) in caerulein-induced acute pancreatitis in mice.

Hydrogen sulfide (H(2)S), 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 H(2)S 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.

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

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.

Zinc mapping and density imaging of rabbit pancreas endocrine tissue sections using nuclear microscopy.

Nuclear microscopy is a suite of techniques based on a focused beam of MeV protons. These techniques have the unique ability to image density and structural variations in relatively thick tissue sections, map trace elements at the cellular level to the microgram per gram (dry weight) level, and extract quantitative information on these elements. The trace elemental studies can be carried out on unstained freeze-dried tissue sections, thereby minimizing any problems of contamination or redistribution of elements during conventional staining and fixing procedures.

Pro-inflammatory effects of hydrogen sulphide on substance P in caerulein-induced acute pancreatitis.

Hydrogen sulphide (H(2)S), a novel gasotransmitter, has been recognized to play an important role in inflammation. Cystathionine-gamma-lyase (CSE) is a major H(2)S synthesizing enzyme in the cardiovascular system and DL-propargylglycine (PAG) is an irreversible inhibitor of CSE. Substance P (SP), a product of preprotachykinin-A (PPT-A) gene, is a well-known pro-inflammatory mediator which acts principally through the neurokinin-1 receptor (NK-1R).

Treatment with H2S-releasing diclofenac protects mice against acute pancreatitis-associated lung injury.

Impaired lung function in severe acute pancreatitis is the primary cause of morbidity and mortality in this condition. Hydrogen sulfide (H(2)S) is a naturally occurring gas that has been shown to be a potent vasodilator. Diclofenac is a nonsteroidal anti-inflammatory drug and has been shown to have anti-inflammatory, analgesic, and antipyretic activity.