ABSORPTION-ENHANCING MECHANISM OF SODIUM CAPRATE AND DECANOYLCARNITINE IN CACO-2 CELLS
Citation
M. Tomita et al., ABSORPTION-ENHANCING MECHANISM OF SODIUM CAPRATE AND DECANOYLCARNITINE IN CACO-2 CELLS, The Journal of pharmacology and experimental therapeutics, 272(2), 1995, pp. 739-743
Categorie Soggetti
Pharmacology & Pharmacy
SICI code
0022-3565(1995)272:2<739:AMOSCA>2.0.ZU;2-V
Abstract
The mechanism of action of the absorption enhancers such as sodium cap
rate (C10) and decanoylcarnitine (DC) was examined. Both C10 and DC in
creased the epithelial permeability of fluorescein isothiocyanate dext
ran 4000 and decreased the transepithelial electrical resistance in Ca
co-2 cell monolayer. irrespective of the presence or absence of mucosa
l calcium, C10 rapidly increased intracellular calcium levels dose-dep
endently. Compound 48/80, a phospholipase C inhibitor, prevented the i
ncreases of the intracellular calcium level and permeability of fluore
scein isothiocyanate dextran 4000 by C10. Furthermore, N-(6-aminohexyl
)-5-chloro-1-naphthalenesulfonamide hydrochloride, a strong calmodulin
inhibitor, also significantly decreased the enhancing effect of C10.
These results suggest that C10 releases calcium from intracellular sto
res via activation of phospholipase C in plasma membrane. The increase
of the calcium levels was considered to induce the contraction of cal
modulin-dependent actin microfilament, followed by dilatation of the p
aracellular route. Although DC also increased intracellular calcium le
vels, neither compound 48/80 nor N-(6-aminohexyt)-5-chloro-1-naphthale
nesulfonamide hydrochloride decreased the enhancing effect of DC. The
enhancing mechanisms were different for C10 and DC.