ЖЕЛЧНЫЕ КИСЛОТЫ КАК ПАТОГЕНЕТИЧЕСКИЙ ФАКТОР ОСТРОГО БИЛИАРНОГО ПАНКРЕАТИТА

Abstract

The review presents an analysis of the literature on the toxic effects of bile acids on the acinar cells of the pancreas as a possible pathogenetic factor in acute biliary pancreatitis. It is shown that at an early stage of acute biliary pancreatitis the damage to the acinar cells is manifested in disturbances of the secretory process, activity of the digestive enzymes, as well as in the disturbances in the structure and function of cell membranes and organelles. It is assumed that the general mechanism that mediates the final death of the acinar cells might be aberrant calcium signaling pathways induced by bile acids. Bile acids can be taken up by the acinar cells through Na+ -dependent and Na+ -independent transporters located at the plasma membrane, or by a G-protein-coupled receptor for bile acids. Cytosolic bile acids induce sustained increase in calcium concentration via mechanisms that involve depletion of intracellular Ca2+ stores and activation of Ca2+ entry. Overload with Ca2+ leads to intracellular trypsinogen activation, mitochondrial depolarization, depletion of ATP and subsequent death of the acinar cells.