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姜黄素对暴露于胆酸的食管上皮细胞的化学保护作用。

Chemoprotective effects of curcumin in esophageal epithelial cells exposed to bile acids.

机构信息

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, USA.

出版信息

World J Gastroenterol. 2010 Sep 7;16(33):4152-8. doi: 10.3748/wjg.v16.i33.4152.

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 micromol/L displayed minimal inhibition of HET-1A cell viability. Deoxycholic acid at a concentration of 200 micromol/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 mumol/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.

摘要

目的

研究姜黄素对抗胆汁酸对食管上皮细胞基因表达影响的能力。

方法

用脱氧胆酸处理食管上皮细胞系(HET-1A),并用姜黄素处理。用细胞增殖和活力测定法确定姜黄素的合适剂量范围。还评估了姜黄素和胆汁酸对环氧化酶-2(COX-2)和超氧化物歧化酶(SOD-1 和 SOD-2)基因表达的联合和单独作用。

结果

在 10-100 微摩尔/升的剂量范围内,姜黄素对 HET-1A 细胞活力的抑制作用最小。与载体对照相比,浓度为 200 微摩尔/升的脱氧胆酸使 COX-2 基因表达增加了 2.4 倍。脱氧胆酸诱导的 COX-2 表达增加部分被姜黄素逆转,姜黄素使 COX-2 表达降低了 3.3-1.3 倍。暴露于胆汁酸的 HET-1A 细胞中 SOD-1 和 SOD-2 基因的表达减少,但高浓度脱氧胆酸(200 微摩尔/升)导致 SOD-2 表达增加 3 倍。用姜黄素处理可部分逆转胆汁酸诱导的所有测试浓度的 SOD-1 表达降低。

结论

姜黄素逆转胆汁酸对 SOD-1 基因表达的抑制。姜黄素还能够抑制胆汁酸诱导的 COX-2 基因表达。

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