论文部分内容阅读
目的研究葛根素肠道吸收的机制,探讨提高其肠道吸收的方法。方法改变实验时间、温度及药物质量浓度,考察葛根素在Caco-2细胞中的转运特性,并考察不同的吸收促进剂对其跨膜转运的影响。结果葛根素的膜渗透性低,被动扩散是其跨膜转运的主要机制;十二烷基磺酸钠(SDS)破坏Caco-2单细胞层的完整性,提高葛根素转运;聚氧乙烯月桂基醚(Brij 35)、牛血清白蛋白(BSA)和分离乳清蛋白对葛根素转运有促进作用,但不影响Caco-2细胞的跨膜电阻(TEER);相对分子质量较高的壳聚糖通过可逆性地降低TEER,促进细胞间转运,提高葛根素的膜渗透性。结论葛根素的膜渗透性低是口服生物利用度低的主要原因,不同吸收促进剂可通过不同机制改善其膜渗透性。
Objective To study the mechanism of puerarin intestinal absorption and to explore ways to improve intestinal absorption. Methods The experimental time, temperature and drug concentration were changed to investigate the transport characteristics of puerarin in Caco-2 cells. The effects of different absorption enhancers on transmembrane transport were also investigated. Results The membrane permeability of puerarin was low and the passive diffusion was the main mechanism of transmembrane transport. Sodium dodecyl sulfate (SDS) destroys the integrity of Caco-2 monolayer and enhances puerarin transport. Polyoxyethylene laurel Brij 35, bovine serum albumin (BSA) and whey protein isolated could promote the transport of puerarin but did not affect the transmembrane resistance (TEER) of Caco-2 cells. The higher relative molecular mass of chitosan Sugar reversibly decreases TEER, promotes cell-to-cell transport, and increases membrane permeability of puerarin. Conclusions Low membrane permeability of puerarin is the main reason for the low oral bioavailability. Different absorption enhancers improve their membrane permeability through different mechanisms.