雷公藤内酯醇对伊马替尼耐药的K562/G01细胞增殖抑制及诱导凋亡作用的研究

本研究旨在探讨雷公藤内酯醇对K562/G01细胞增殖抑制和诱导凋亡作用的影响及其可能的机制.MTT法检测伊马替尼、雷公藤内酯醇单药及联合用药对K562/G01增殖的影响；流式细胞术检测细胞周期、细胞凋亡率和P-gp蛋白表达的变化；Western blot分析P-gp蛋白的表达情况；实时荧光定量PCR检测BCR/ABL基因的表达.结果表明：雷公藤内酯醇能增强伊马替尼对K562/G01细胞的增殖抑制和诱导凋亡作用；雷公藤内酯醇能将细胞阻滞在G1期,下调P-gp蛋白和BCR/ABL基因表达.结论：雷公藤内酯醇对K562/G01细胞有增殖抑制和诱导凋亡作用,其机制可能与细胞周期的G1期阻滞、降低P-gp蛋白表达和抑制BCR/ABL基因表达有关.

Triptolide Inhibits Proliferation and Iuduces Apoptosis of Imatinib Resistant K562/G01 cells

This study was aimed to explore the inhibitory effect of triptolide on proliferation and inducing apoptosis effect of K562/G01 cells and their possible mechanism. MTT assay was used to detect the effect of imatinib or triptolide alone and their combination on K562/G01 proliferation; the cell cycle, apoptosis rate, P-gp protein expression were detected by folw cytometry （FCM）; the expression of P-gp was assessed by Western blot; the BCR/ABL gene expression was assayed by real time guantitative PCR. The results showed that triptolide could enhance the effect of imatinib on proliferation inhibition and apoptosis of K562/G01, arrested the cell cycle in G1 phase, down-regulated the expression of BCR/ABL gene and P-gp protein. It is concluded that triptolide induces K562/G01 cell proliferation inhibition and apoptosis, the mechanism may be related to cell cycle arrest, decrease of P-gp protein expression, inhibition of BCR/ABL gene expression.