中文摘要：

目的：通过多种不同细胞模型研究两种芪类天然化合物白藜芦醇（trans-resveratrol,TR）及白藜芦醇苷（trans-piceid,TP）与多种药物外排转运体间的相互作用。方法：高效液相及荧光分光光度法分别测定细胞内TR、TP及罗丹明123的浓度,MTT比色法测定细胞活性,Western blot法测定P-糖蛋白的表达。结果：P-糖蛋白抑制剂及底物（维拉帕米和罗丹明123）对TR及TP的细胞摄取无影响。多药耐药相关蛋白2抑制剂,丙磺舒可将TR及TP的细胞摄取量分别增加1.3倍和1.6倍。TR及TP能够显著性增加大鼠脑微血管细胞对罗丹明123的摄取及阿霉素在人白血病阿霉素耐药细胞上的毒性,但对人白血病阿霉素耐药细胞上P-糖蛋白的表达没有显著性改变。米托蒽醌在人非小细胞肺癌细胞上的毒性作用不受TR及TP的影响。结论：TR及TP可以抑制P-糖蛋白的外排作用,但其本身不被P-糖蛋白外排,而是被多药耐药相关蛋白2外排。TR及TP对人乳腺癌多药耐药蛋白的外排作用没有影响。

英文摘要：

AIM： To study the two stilbenes＇ （trans-resveratrol, TR and its glucoside trans-piceid, TP） interaction with ABC transporters in cell models. METHODS： The concentrations of TR, TP, and Rhodamine 123 （Rh123） in ceils were measured by HPLC or fluorescence spectrophotometer. Cytotoxicity was determined with MTT. The expression of P-gp was evaluated using Western blot. RESULTS： P-gp＇s in- hibitor and substrate （Verapamil and Rh123） had no impact on the accumulation of the two stilbenes. Probenecid, the inhibitor of muhidrug resistance-associated protein-2 （Mrp-2）, increased accumulation of TR and TP to 1.3 and 1.6 folds. TR and TP increased the uptake of Rh123 in RBMECs. Adriamycin＇ s （ADM） cytotoxicity was also enhanced by the two stilbenes. The expression of P-gp in K562/A02 cells wasn＇ t changed noticeably by co-incubating with TR or TP. The stilbenes also didn＇ t change the cytotoxicity of Mi- toxantrone （MIT） in Human non-small cell lung cancer cell （NCI-H460）. CONCLUSION： TR and TP inhibited P-gp from excreting substrates. They were effluent by Mrp-2, not P-gp. They didn＇t affect the effluent of BCRP.