【摘要】 目的:探讨姜黄素(Cur)对人结肠癌耐奥沙利铂(Oxa)细胞株(SW620/OxR)的逆转耐药作用及其机制是否与抑制STAT3信号通路有关。方法:采用WST-1试剂检测Cur对SW620/OxR细胞株的半数抑制(IC50)浓度,选择IC50低一浓度梯度的Cur+2μmol/L Oxa作用于SW620/OxR细胞48 h(称为实验组),与仅加入2μmol/L的Oxa对照组比较,1采用流式细胞术检测细胞凋亡;2采用Western blot检测STAT3活化标志磷酸化STAT3(P-STAT3)蛋白及其下游耐药相关靶分子P糖蛋白(P-gp)的表达情况。结果:Cur对SW620/OxR细胞的IC50浓度为18.9μmol/L;实验组与对照组比较:1细胞凋亡率由(5.08±1.82)%上升到(30.69±2.94)%,实验组细胞凋亡率明显高于对照组(P<0.05);2P-STAT3及P-gp表达量均明显受抑制(P<0.05)。结论:Cur具有调控人结肠癌耐药细胞株耐药性的作用,可能与抑制STAT3信号通路,降低P-gp表达有关。更多还原

【Abstract】 Objective: To investigate the reversal multidrug resistance effects of curcumin on human colorectal cancer cell lines resistant to oxaliplatin( SW620 / OxR) and whether its mechanism was involved in downregulation of STAT3 signaling. Methods: The IC50 value( 50% cell growth inhibitory concentrations) of curcumin to SW620 / OxR cell lines was obtained by WST-1 reagent,which was one kind of cell proliferation assay. Later experiments included in the experimental group and the control group. In the experimental group,SW620 / OxR cell lines were exposed to the previous experiment IC50 concentrations of curcumin plus 2 μmol / L oxaliplatin for48 h,while in the control group,SW620 / OxR cell lines were cultured in medium containing in 2 μmol / L oxaliplatin. In the two groups:apoptosis was detected by flow cytometry; the protein expression levels of phosphorylated STAT3( P-STAT3) and P-gp were disclosed by Western blot. Results: The IC50 value of curcumin to SW620 / OxR cell lines was 18. 9 μmol / L. The apoptosis rate of cells in the control group and the experimental group were respectively( 5. 08 ± 1. 82) % and( 30. 69 ± 2. 94) %,the apoptosis rate of the experimental group was significantly higher than that of the control group( P < 0. 05). The protein expression levels of phosphorylated STAT3( PSTAT3) and P-gp in the experimental group was significantly lower than that in the control group( P < 0. 05). Conclusion: Curcumin can reverse drug resistance in colorectal cancer cell lines resistant to oxaliplatin,its effect may be associated with downregulation of STAT3 signaling pathways.更多还原