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 ($0.1-1{mu}M$) dose-dependently increased intracellular $Ca^{2+}$ mobilization in the presence of extracellular $Ca^{2+}$, but was not affected by $1{mu}M$ U73122, a specific PLC inhibitor. In the absence of extracellular $Ca^{2+}$, melittin ($1{mu}M$) 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 ($10{mu}M$) significantly inhibited $1{mu}M$ melittin-induced $Ca^{2+}$ mobilization by 33 %. In [$^3H$]inositol-labeled cells, $1{mu}M$ melittin did not increase inositol phosphate formation, but more than $5{mu}M$ melittin significantly increased inositol phosphate formation, which was significantly inhibited by acteoside. Melittin ($1{mu}M$) significantly increased histamine release from RBL 2H3 cells in the presence or absence of extracellular$Ca^{2+}$. Acteoside significantly inhibited $1-{mu}M$-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 $1{mu}M$-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.