Biotransformation of ginsenoside Rb1 via the gypenoside pathway by human gut bacteria
Biotransformation of ginsenoside Rb1 via the gypenoside pathway by human gut bacteria
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人类肠道细菌通过绞股蓝皂苷途径生物转化人参皂苷 Rb1
DOI：
10.1186/1749-8546-8-22
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发表时间：
2013-11-23
期刊：
影响因子：
4.9
通讯作者：
Yan, Ru
中科院分区：
文献类型：
--
作者：
Shen, Hong;Leung, Weng-Im;Yan, Ru
背景：人参皂苷的细菌转化对人参皂苷的健康促进作用至关重要。以往关于肠道细菌转化人参皂苷Rb1 （Rb1）的研究主要集中在人参皂苷Rd （Rd）途径（Rb1）上。人参皂苷F2 （F2）。化合物K (Cpd K))。本研究旨在探讨绞股蓝皂苷在体外人肠道细菌中的途径。方法：通过与健康志愿者肠道菌群共孵育或单独孵育，研究人参皂苷Rb1及其代谢产物人参皂苷Rd和绞股皂苷XVII在人体肠道菌群中的代谢途径。采用LC/MSD Trap系统在负离子模式下定性分析人参皂苷Rb1、人体肠道细菌产生的代谢产物以及模拟胃液（SGF）中的降解产物，并采用HPLC-UV分析定量测定。结果：与肠道菌群厌氧培养时，Rb1产生5种代谢物，分别为Rd、F2、cppd K和罕见的绞股皂苷XVII （G-XVII）和LXXV （G-LXXV）。绞股蓝苷途径(Rb1；G-XVII。G-LXXV。cppd K)是快速、中间和次要的，最终通过G-XVII将Rb1转化为cppd K。F2（主修）/G-LXXV（副修）。Rd途径和绞股蓝苷途径在年龄和性别无关的个体间差异较大（P < 0.05）。Rb1具有很强的酸不稳定性，可快速降解生成F2、人参皂苷Rg3、人参皂苷Rh2和cppd K，但在SGF中不生成绞股蓝皂苷。绞股蓝皂苷的形成可能是由肠道细菌介导的酶促过程所引起的。结论：Rb1在体外可被人肠道细菌代谢为G-XVII、F2（主要）或G-LXXL（次要），最终代谢为cppd K。
Background: Bacterial conversion of ginsenosides is crucial for the health-promoting effects of ginsenosides. Previous studies on the biotransformation of ginsenoside Rb1 (Rb1) by gut bacteria have focused on the ginsenoside Rd (Rd) pathway (Rb1. Rd. ginsenoside F2 (F2). compound K (Cpd K)). This study aims to examine the gypenoside pathway in human gut bacteria in vitro.Methods: The metabolic pathways of ginsenoside Rb1 and its metabolites ginsenoside Rd and gypenoside XVII in human gut bacteria were investigated by incubating the compounds anaerobically with pooled or individual gut bacteria samples from healthy volunteers. Ginsenoside Rb1, the metabolites generated by human gut bacteria, and degraded products in simulated gastric fluid (SGF) were qualitatively analyzed using an LC/MSD Trap system in the negative ion mode and quantitatively determined by HPLC-UV analysis.Results: When incubated anaerobically with pooled gut bacteria, Rb1 generated five metabolites, namely Rd, F2, Cpd K, and the rare gypenosides XVII (G-XVII) and LXXV (G-LXXV). The gypenoside pathway (Rb1. G-XVII. G-LXXV. Cpd K) was rapid, intermediate, and minor, and finally converted Rb1 to Cpd K via G-XVII. F2 (major)/G-LXXV (minor). Both the Rd and gypenoside pathways exhibited great inter-individual variations in age-and sex-independent manners (P > 0.05). Rb1 was highly acid-labile and degraded rapidly to form F2, ginsenoside Rg3, ginsenoside Rh2, and Cpd K, but did not generate the gypenosides in SGF. The formation of the gypenosides might be explained by the involvement of a gut bacteria-mediated enzymatic process.Conclusions: Rb1 was metabolized to G-XVII, F2 (major) or G-LXXL (minor), and finally Cpd K by human gut bacteria in vitro.