The effect of acteoside on intracellular Ca2+ mobilization and phospholipase C activity in RBL-2H3 cells stimulated by melittin

Abstract

This study was performed to investigate the effects of acteoside on various cellular functions such as, intracellular Ca(2+) mobilization, phospholipase C activity, and exocytosis induced by melittin. Melittin (0.1-1μM) dose-dependently increased intracellular Ca(2+) mobilization in the presence of extracellular Ca(2+), but was not affected by 1μM U73122, a specific PLC inhibitor. In the absence of extracellular Ca(2+), melittin (1μM) did not induce a change in intracellular Ca(2+) mobilization, which suggests that melittin-induced intracellular Ca(2+) mobilization may be dependent on the influx of extracellular Ca(2+) rather than on the release of intracellular Ca(2+) storage. Acteoside (10μM) significantly inhibited 1μM melittin-induced Ca(2+) mobilization by 33%. In [(3)H]inositol-labeled cells, 1μM melittin did not increase inositol phosphate formation, but more than 5μM melittin significantly increased inositol phosphate formation, which was significantly inhibited by acteoside. Melittin (1μM) significantly increased histamine release from RBL 2H3 cells in the presence or absence of extracellular Ca(2+). Acteoside significantly inhibited 1-μM-melittin-induced histamine release by 74% in the presence of extracellular Ca(2+) and by 71% in the absence of extracellular Ca(2+). These data suggest that the inhibitory effect of acteoside on 1μM-melittin-induced histamine release may be related to blockage of the calcium-independent pathway. Taken together, these data suggest that melittin has an influence on cellular functions such as intracellular Ca(2+) mobilization, the PLC pathway, and exocytosis via various independent signalling pathways in RBL-2H3 cells, and was significantly inhibited by acteoside.