摘要
目的观察黄连素对脱氧胆酸(DCA)诱导的人结肠癌HT-29细胞增殖的抑制作用,探讨其可能的机制。方法200/μmol/LDCA加到HT-29细胞培养液中,同时给予不同浓度黄连素(1、5、10和20μmol/L),采用MTT法测定细胞增殖；RT-PCR法检测环氧合酶-2(COX-2)mRNA,免疫组化染色法检测细胞COX-2表达,放免法检测前列腺素E2(PGE2)含量。采用t检验和单因素方差分析。结果DCA作用HT-29细胞6 h,COX-2蛋白表达阳性率较对照组明显升高(65．5%±5．6%比6．2%±1．1%),PGE2合成增加(24．1 ng/L±1．4 ng/L比10．6 ng/L±0．8 ng/L),1μmol/L黄连素对DCA诱导的HT-29细胞作用6 h可抑制细胞增殖,抑制率为7．4%±3．5%。黄连素浓度≥1μmol/L时,可抑制DCA诱导的COX-2 mRNA表达,并抑制PGE2合成,上述作用均呈浓度-时间依赖性。结论黄连素可抑制DCA诱导的HT-29人结肠癌细胞增殖,抑制COX-2 mRNA和蛋白表达及PGE2合成,这可能是黄连素抑制HT-29细胞增殖的机制之一。
Objective To investigate the effect of berberine on inhibiting HT-29 human colon cancer cell proliferation induced by deoxycholic acid （DCA）. Methods The berberine with concentration of 1, 5, 10 or 20μmol/L were added into the HT-29 human colon cancer cell culture media containing 200μmol/L DCA. The effects of berberine on cell proliferation were studied by the method of MTT. RT-PCR was applied to measure the expression of cyclooxygenase-2 （COX-2） mRNA. Cellular immunochemical stain was applied to label COX- 2 protein expression. Concentration of prostaglandin E2 （PGE2） was measured by radioimmunoassay. Results HT-29 cells were incubated with DCA for 6 h, COX-2 expression of cells were increased prominent compared to controls （65.5%±5.6% vs. 6.2%±1.1%）. The level of PGE2 were increased （24. 1 ng/L ±1.4 ng/L vs. 10. 6 ng/L±0.8 ng/L）. One μmol/L berberine reduced the proliferation rate of HT-29 induced by DCA over 6 h, the proliferation rate was 7.4%±3.5%. Both COX-2 mRNA expression and the level of PGE2 were inhibited when the concentration of berberine was over 1 μmol/L, and in a concentration-time dependent manner. Conclusions Berberine can inhibit the proliferation of HT-29 human colon cancer cell induced by DCA. Berberine can also suppress the expression of COX-2, and decrease the production of PGE2. These data provide new insights into the mechanism of its anti-cancer properties.
出处
《中华消化杂志》
CAS
CSCD
北大核心
2006年第11期749-752,共4页
Chinese Journal of Digestion
