Dual Effect of the Anti-Allergic Astemizole on Ca2 Fluxes in Rat Basophilic Leukemia (RBL-2H3) Cells: Release of Ca2 from Intracellular Stores and Inhibition of Ca2 Release-Activated Ca2 Influx

Licochalcones suppress degranulation by decreasing the intracellular Ca2+ level and tyrosine phosphorylation of ERK in RBL-2H3 cells

“…These results suggested that Lico D may inhibit mast cell degranulation via inhibition of Ca 2+ influx. This assumption is supported by previous reports that some anti-allergic drugs inhibit mast cell degranulation via inhibition of Ca 2+ influx [28][29][30][31][32]. While 10 μM Lico D did not show inhibitory effect on ionomycin-induced Ca 2± influx, it significantly inhibited ionomycin-induced mast cell degranulation in RBL-2H3 cells.…”

Relocalization of STIM1 in mouse oocytes at fertilization: early involvement of store-operated calcium entry

“…This opening of SOC channels can be followed by employing calcium or barium addition to the extracellular medium. Barium (Ba 2C ) has been shown to enter the cell via SOC channels in other cell types (Hoth 1995, Fischer et al 1998, as well as in oocytes (Martin-Romero et al 2008), but cannot be extruded by PM calcium pumps. Since fura-2 is also sensitive to Ba 2C , this offers a useful tool with which to reveal the occurrence of SOCE.…”

Mechanism of action of the nonlipophilic antiallergic drug eclazolast (REV 2871) in the inhibition of mediator release in a mast cell model

“…Furthermore, eclazolast does not inhibit extracellular Ca 2+ influx directly as appears from the lack of effect on TG induced Ca 2+ influx. Apparently, eclazolast has no influence on the SOC channels [23] as observed for oxatomide and astemizole [7,[14][15]. Additionally, eclazolast has no effect on the release of b-hexosaminidase induced by an independent trigger of Ca 2+ influx using the ionophore A23187 (data not shown).…”

“…The curve consists of two phases: the rapid increase is largely due to depletion of IP 3 sensitive Ca 2+ stores, and the sustained phase is due to Ca 2+ influx and efflux. The latter either by efflux over the plasma membrane, or by re-uptake into the stores [7,17]. After treatment of the cells, with increasing eclazolast concentration, two effects are observed (Fig.…”

“…The effects on Ca 2+ influx appeared to be related to distortion of the membrane bilayer [6][7][8]. As membrane distortion is a property related to insertion of the lipophilic drug into the bilayer, the question arises whether the mechanism of action of eclazolast is different from that of lipophilic antiallergics.…”