The role of intracellular calcium in the production of Superoxide anion by Kupffer cells stimulated by lipopolysaccharide and the efficacy of prostaglandin E

Abstract

Abstract Kupffer cells stimulated by lipopolysaccharide (LPS) produce Superoxide anion and cause hepatocellular injury. Intracellular calcium has been noted to work as a second messenger in a variety of pathophysiological mechanisms. The aims of this study were to investigate the effect of LPS stimulation of Kupffer cells on intracellular calcium concentrations and the production of Superoxide anion, and determine the effect of prostaglandin E 1 (PGE 1 ) on intracellular calcium and the Superoxide anion production following stimulation with LPS. Kupffer cells were isolated from male Wistar rats. The intracellular calcium level and the production of Superoxide anion were measured using a fluorescence computed microscope (Mu-1000, Inter Dec) and a Luminescence Reader (BLR-103, Aloka). After LPS stimulation, the intracellular calcium level of Kupffer cells increased and pretreatment with PGE 1 reduced this increase. Pretreatment with PGE 1 and removal of extracellular calcium decreased the production of Superoxide anion from Kupffer cells stimulated by LPS. We conclude that an increase of intracellular calcium affects production of Superoxide anion from Kupffer cells stimulated by LPS. Pretreatment with PGE 1 reduces the production of Superoxide anion by preventing this rise in intracellular calcium.