Molecular mechanisms of caffeine-mediated intestinal epithelial ion transports

British Journal of Pharmacology
Fenglian ZhangHui Dong

Abstract

As little is known about the effect of caffeine, one of the most widely consumed substances worldwide, on intestinal function, we aimed to study its action on intestinal anion secretion and the underlying molecular mechanisms. Anion secretion and channel expression were examined in mouse duodenal epithelium by Ussing chambers and immunocytochemistry. Ca2+ imaging was also performed in intestinal epithelial cells (IECs). Caffeine (10 mM) markedly increased mouse duodenal short-circuit current (Isc ), which was attenuated by a removal of either Cl- or HCO3- , Ca2+ -free serosal solutions and selective blockers of store-operated Ca2+ channels (SOC/Ca2+ release-activated Ca2+ channels), and knockdown of Orai1 channels on the serosal side of duodenal tissues. Caffeine induced SOC entry in IEC, which was inhibited by ruthenium red and selective blockers of SOC. Caffeine-stimulated duodenal Isc was inhibited by the endoplasmic reticulum Ca2+ chelator (N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine), selective blockers (ruthenium red and dantrolene) of ryanodine receptors (RyR), and of Ca2+ -activated Cl- channels (niflumic acid and T16A). There was synergism between cAMP and Ca2+ signalling, in which cAMP/PKA promoted caffeine/Ca2...Continue Reading

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