Econazole depleted calcium release-activated calcium (CRAC) current through blockade of voltage-dependent Ca2+channels = Econazol menghambat calcium release-activated calcium (CRAC) current melalui penghambatan ..
| Main Author: | Perpustakaan UGM, i-lib |
|---|---|
| Format: | Article NonPeerReviewed |
| Terbitan: |
[Yogyakarta] : Universitas Gadjah Mada
, 2011
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| Subjects: | |
| Online Access: |
https://repository.ugm.ac.id/28918/ http://i-lib.ugm.ac.id/jurnal/download.php?dataId=11981 |
Daftar Isi:
- Econazole is an azole antifungal agent which can block the calcium release-activated calcium (CRAC) current in human leukaemic T cell line. The phenomenon is also possible to occur in mast cell such as RBL-2H3 (rat basophilic leukemia) cells, a tumor:: analog of mast cells. In the study, we investigated effect of econazole on 4SCa2+uptake into the cells in response to thapsigargin, an ATP-dependent Ca2+(SERCA)inhibitor, by direct measurement radiolabelled Ca2+uptake in cells. The mechanism underlying this effect of econazole was studied using molecular modelling. In present study, econazole inhibited 4SCa2+influx into mast cells in absence of mast cells inducer, thapsigargin. Moreover, econazole potently suppressed the 4SCa2+influx induced by thapsigargin. It was supported that econazole also inhibited Ca2+- induced tracheal contraction. The increase of Ca2+ was stimulated by the opening of voltage-dependent Ca2+channels activated by KCl-induced membrane depolarization. Based on molecular docking study, score of interaction (equal energy of interaction) of 3FGO, a main protein target on Ca2+-ATPase, with native ligan, thapsigargin and econazole were -76.941, -117.205, and -92.277, respectively. The interaction of thapsigargin and Ca2+-ATPasewas more stable than this of econazole and Ca2+-ATPase. It suggests that it would be difficult econazole to block the interaction of thapsigargin with Ca2+-ATPase to increase intracellular Ca2+. In conclusion, econazole inhibited the increase of intracellular Ca2+involving the blokade of voltage-dependent Ca2+channels, but involving the Ca2+-ATpasepathway.