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Curcumin does not stimulate cAMP-mediated chloride transport in cystic fibrosis airway epithelial cells.

Abstract：

:It has been suggested that curcumin and other sarcoplasmic/endoplasmic reticulum Ca(2+)-pump inhibitors could correct the defect in the most common mutation (DeltaF508) in cystic fibrosis (CF), and restore normal chloride transport. In the present study, the effect of curcumin was tested on baby hamster kidney (BHK) cells transfected with DeltaF508-CFTR, a CF airway epithelial cell line (CFBE), and cells isolated from the nasal epithelium of CF-patient homozygous for the DeltaF508-mutation. Curcumin had a small effect on basal (non-CFTR-mediated) chloride efflux in CFBE and CF nasal epithelial cells, but did not increase the net cAMP-activated (CFTR-mediated) chloride efflux. Curcumin caused a small increase in net cAMP-activated chloride efflux from DeltaF508-CFTR BHK cells. Immunocytochemical analysis failed to show significant movement of DeltaF508-CFTR to the plasma membrane in DeltaF508-CFTR BHK cells or CFBE cells. It is concluded that it is unlikely that curcumin has a significant positive effect on CFTR-mediated chloride transport in airway epithelial cells.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Dragomir A,Björstad J,Hjelte L,Roomans GM

doi

10.1016/j.bbrc.2004.07.146

subject

Has Abstract

pub_date

2004-09-17 00:00:00

pages

447-51

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(04)01623-7

journal_volume

322

pub_type

杂志文章

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