目的 研究乳香提取物中3-乙酰基-11-羰基-β-乙酰乳香酸（AKBA）在Caco-2、MDCK-MDR1和MDCK-Wild细胞模型中的吸收转运机制。方法 利用Caco-2、MDCK-MDR1和MDCK-Wild细胞模型，研究AKBA由细胞层顶端（AP）→基底端（BL）和BL→AP的双向转运过程；采用LC-MS/MS法测定AKBA的量，计算表观渗透系数（P_app）。结果 在Caco-2细胞模型中，50 μmol/L AKBA 由AP→BL、BL→AP的P_app分别为7.9×10^?7、1.5×10^?7 cm/s，在MDCK-MDR1细胞模型中，50 μmol/L AKBA由AP→BL、BL→AP的P_app分别为2.6×10^?7、0.8×10^?7 cm/s，在MDCK-Wild细胞模型中，50μmol/L AKBA由AP→BL、BL→AP的P_app分别为2.4×10^?7、0.6×10^?7 cm/s，3种细胞模型中外排率均小于2。结论 AKBA在肠道中吸收不良，不是P-糖蛋白的底物，推测其通过摄入型主动转运和被动扩散两种机制透过小肠上皮细胞。

Objective To study the mechanisms of absorption and transport of 3-acetyl-11-keto-β-boswellic acid (AKBA) from Boswellia carterif in Caco-2 cell, MDCK-MDR1, and MDCK-Wild cell models. Methods The Caco-2, MDCK-MDR1, and MDCK-Wild cell monolayer models were used to study the bi-directional transport of AKBA in apical (AP)→basal (BL) or BL→AP; The concentration of AKBA was measured by LC-MS/MS and apparent permeability coefficient (P_app) was calculated. Results P_app (AP→BL) and P_app (BL→AP) values of AKBA (50 μmol/L) in Caco-2 cell model were 7.9 × 10^?7 and 1.5 × 10^?7 cm/s, respectively; P_app (AP→BL) and P_app (BL→AP) values of AKBA (50 μmol/L) in MDCK-MDR1 cell model were 2.6 × 10^?7 and 0.8 × 10^?7 cm/s, respectively; P_app (AP→BL) and P_app (BL→AP) of AKBA (50 μmol/L) in MDCK-Wild cell model was 2.4 × 10^?7 and 0.6 × 10^?7 cm/s, respectively; The rates of efflux (R_E) for AKBA in Caco-2 and MDCK-MDR1 cell monolayers were both smaller than 2. Conclusion AKBA is not the substrate of P-gp and its absorption rate is low. AKBA is absorbed through the intestinal epithelial cells by active transport absorption and passive diffusion possibly.

国家“重大新药创制”科技重大专项—新药临床前药物代谢动力学技术平台建设（2012ZX09304002）；国家“973”项目（2010CB735602）