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Gintonin absorption in intestinal model systems

机译：肠道模型系统中人参皂苷的吸收

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Background Recently, we identified a novel ginseng-derived lysophosphatidic acid receptor ligand, called gintonin. We showed that gintonin induces [Ca2+]i transient-mediated morphological changes, proliferation, and migration in cells expressing lysophosphatidic acid receptors and that oral administration of gintonin exhibits anti-Alzheimer disease effects in model mice. However, little is known about the intestinal absorption of gintonin. The aim of this study was to investigate gintonin absorption using two model systems. Methods Gintonin membrane permeation was examined using a parallel artificial membrane permeation assay, and gintonin absorption was evaluated in a mouse everted intestinal sac model. Results The parallel artificial membrane permeation assay showed that gintonin could permeate an artificial membrane in a dose-dependent manner. In the everted sac model, gintonin absorption increased with incubation time (from 0?min to 60?min), followed by a decrease in absorption. Gintonin absorption into everted sacs was also dose dependent, with a nonlinear correlation between gintonin absorption and concentration at 0.1–3?mg/mL and saturation at 3–5?mg/mL. Gintonin absorption was inhibited by the Rho kinase inhibitor Y-27632 and the sodium–glucose transporter inhibitor phloridzin. Moreover, lipid extraction with methanol also attenuated gintonin absorption, suggesting the importance of the lipid portion of gintonin in absorption. This result shows that gintonin might be absorbed through passive diffusion, paracellular, and active transport pathways. Conclusion The present study shows that gintonin could be absorbed in the intestine through transcellular and paracellular diffusion, and active transport. In addition, the lipid component of gintonin might play a key role in its intestinal absorption.
机译：背景技术最近，我们鉴定了一种新的人参来源的溶血磷脂酸受体配体，称为人参皂苷。我们表明，人参皂甙诱导表达溶血磷脂酸受体的细胞中[Ca 2 + ] i瞬时介导的形态学变化，增殖和迁移，并且人参皂甙口服给药对模型小鼠具有抗阿尔茨海默病的作用。但是，关于金精素在肠内的吸收知之甚少。这项研究的目的是使用两种模型系统研究人参皂苷的吸收。方法采用平行人工膜渗透测定法检测人参皂苷膜的渗透性，并在小鼠外翻肠囊模型中评估人参皂苷的吸收。结果平行人工膜渗透试验表明，人参皂苷可以剂量依赖性方式渗透人工膜。在外翻囊模型中，随着培养时间的延长（从0？min到60？min），人参素的吸收增加，随后吸收减少。浸润囊中的金精蛋白吸收也是剂量依赖性的，在0.1–3？mg / mL的浓度和3–5？mg / mL的饱和度之间，金尿素的吸收与浓度之间存在非线性关系。 Rho激酶抑制剂Y-27632和钠-葡萄糖转运蛋白抑制剂phloridzin抑制金精蛋白的吸收。此外，用甲醇进行脂质提取也减弱了人参皂苷的吸收，表明人参皂苷的脂质部分在吸收中的重要性。该结果表明，人参素可能通过被动扩散，细胞旁和主动转运途径被吸收。结论本研究表明，gintinin可通过跨细胞和旁细胞扩散以及主动转运而在肠道中被吸收。此外，gintinin的脂质成分可能在其肠道吸收中起关键作用。

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