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

Biochem Biophys Res Commun. 2004 Sep 17;322(2):447-51. doi: 10.1016/j.bbrc.2004.07.146.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chlorides / metabolism*
  • Cricetinae
  • Curcumin / pharmacology*
  • Cyclic AMP / metabolism*
  • Cystic Fibrosis / drug therapy*
  • Cystic Fibrosis Transmembrane Conductance Regulator / drug effects*
  • Enzyme Inhibitors / pharmacology*
  • Fluorescent Antibody Technique
  • Humans
  • Immunohistochemistry
  • Respiratory Mucosa / metabolism*


  • CFTR protein, human
  • Chlorides
  • Enzyme Inhibitors
  • Cystic Fibrosis Transmembrane Conductance Regulator
  • Cyclic AMP
  • Curcumin