Bioactive dietary polyphenolic compounds reduce nonheme iron transport across human intestinal cell monolayers
Bioactive dietary polyphenolic compounds reduce nonheme iron transport across human intestinal cell monolayers
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DOI：
10.1093/jn/138.9.1647
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发表时间：
2008-09-01
影响因子：
4.2
通讯作者：
Han, Okhee
中科院分区：
文献类型：
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作者：
Kim, Eun-Young;Ham, Soo-Kyung;Han, Okhee
有令人信服的流行病学证据表明，经常摄入膳食中具有生物活性的多酚类化合物可促进人体健康。由于膳食多酚化合物在体内和体外具有广泛的作用，包括对铁等金属的螯合作用，因此测试经常食用生物活性多酚成分是否会损害膳食铁的利用是谨慎的。我们研究了日粮多酚(-)-表没食子儿茶素-3-没食子酸酯（EGCG）和葡萄籽提取物（GSE）对Caco-2肠细胞上皮铁转运的影响，本研究中使用的EGCG和GSE浓度范围在生理水平范围内，不影响分化的Caco-2细胞单层的完整性。EGCG和GSE均能降低经膈铁转运（P < 0.001）。然而，添加EGCG和GSE增加了根尖铁的摄取（P < 0.001）。铁摄取的增加可能部分是由于EGCG和GSE活性的降低。EGCG和GSE都减少了吸收缓冲液中15%的Fe3+。尽管55铁的细胞水平增加，但铁在肠细胞基底外侧膜上的转移极低，表明通过铁转运蛋白-1的基底外侧出口受损，可能是通过形成不可运输的多酚-铁复合物。我们的数据表明，多酚通过减少肠细胞的基底外侧铁出口而不是通过减少肠细胞的顶端铁进口来抑制非血红素铁的吸收。
There is persuasive epidemiological evidence that regular intake of dietary bioactive polyphenolic compounds promotes human health. Because dietary polyphenolic compounds have a wide range of effects in vivo and vitro, including chelation of metals such as iron, it is prudent to test whether the regular consumption of bioactive polyphenolic components impair the utilization of dietary iron. We examined the influence of the dietary polyphenols (-) -epigallocatechin-3-gallate (EGCG) and grape seed extract (GSE) on transepithelial iron transport in Caco-2 intestinal cells, The range of EGCG and GSE concentrations used in this study was within physiological levels and did not affect the integrity of differentiated Caco-2 cell monolayers. Both EGCG and GSE decreased (P < 0.001) transepithlial iron transport. However, apical iron uptake was increased (P < 0,001) by the addition of EGCG and GSE. The increased uptake of iron might be due in part to the reducing activity of EGCG and GSE. Both EGCG and GSE reduced similar to 15% of the applied Fe3+ to Fe2+ in the uptake buffer. Despite the increased cellular levels of 55 Fe, the transfer of iron across the basolateral membrane of the enterocyte was extremely low, indicating that basolateral exit via ferroportin-1 was impaired, possibly through formation of a nontransportable polyphenol-iron complex, Our data show that polyphenols inhibit nonheme iron absorption by reducing basolateral iron exit rather than by decreasing apical iron import in intestinal cells.