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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(HET1A)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 10-100μmol/L displayed minimal inhibition of HET-1A cell viability.Deoxycholic acid at a concentration of 200μmol/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 200μmol/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.
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 (HET1A) 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 also also displayed. in a dose range of 10-100 μmol / L showed 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. COX-2 induced by deoxycholic acid was created by the addition of curcumin, and curcumin reduced COX-2 expression 3.3-to 1.3-fold. HE-1A cells exposed to bile acid yielded reduced expression of SOD-1 and SOD-2 genes with the exception that high dose of deoxycholic acid at 200 μmol / L led to a 3-fold increase in SOD-2 expression. The addition of curcumin treatment from the 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.