Brief Article
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World J Gastroenterol. Sep 7, 2010; 16(33): 4152-4158
Published online Sep 7, 2010. doi: 10.3748/wjg.v16.i33.4152
Chemoprotective effects of curcumin in esophageal epithelial cells exposed to bile acids
Matthew R Bower, Harini S Aiyer, Yan Li, Robert CG Martin
Matthew R Bower, Harini S Aiyer, Yan Li, Robert CG Martin, Division of Surgical Oncology, Department of Surgery and James Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY 40202, United States
Author contributions: Bower MR and Aiyer HS designed and performed the research, prepared the manuscript; Martin RCG supervised the research design and manuscript preparation; Li Y supervised the design and performance of the research.
Supported by National Institutes of Health Grant, No. 1R03CA137801
Correspondence to: Robert CG Martin, MD, PhD, Division of Surgical Oncology, Department of Surgery and James Graham Brown Cancer Center, University of Louisville School of Medicine, 315 East Broadway - Rm 313, Louisville, KY 40202, United States. robert.martin@louisville.edu
Telephone: +1-502-6293355 Fax: +1-502-6293030
Received: February 9, 2010
Revised: March 28, 2010
Accepted: April 4, 2010
Published online: September 7, 2010
Abstract

AIM: To investigate the ability of curcumin to counteract the impact of bile acids on gene expression of esophageal epithelial cells.

METHODS: An esophageal epithelial cell line (HET-1A) was treated with curcumin in the presence of deoxycholic acid. Cell proliferation and viability assays were used to establish an appropriate dose range for curcumin. The combined and individual effects of curcumin and bile acid on cyclooxygenase-2 (COX-2) and superoxide dismutase (SOD-1 and SOD-2) gene expression were also assessed.

RESULTS: Curcumin in a dose range of 10-100 μmol/L displayed minimal inhibition of HET-1A cell viability. Deoxycholic acid at a concentration of 200 μmol/L caused a 2.4-fold increase in COX-2 gene expression compared to vehicle control. The increased expression of COX-2 induced by deoxycholic acid was partially reversed by the addition of curcumin, and curcumin reduced COX-2 expression 3.3- to 1.3-fold. HET-1A cells exposed to bile acid yielded reduced expression of SOD-1 and SOD-2 genes with the exception that high dose deoxycholic acid at 200 μmol/L led to a 3-fold increase in SOD-2 expression. The addition of curcumin treatment partially reversed the bile acid-induced reduction in SOD-1 expression at all concentrations of curcumin tested.

CONCLUSION: Curcumin reverses bile acid suppression of gene expression of SOD-1. Curcumin is also able to inhibit bile acid induction of COX-2 gene expression.

Keywords: Esophageal cancer; Curcumin; Cyclooxygenase-2; Superoxide dismutase; Chemoprevention