Am J Pathol：绿茶和膳食铁不宜同时摄入
2016/6/25 0:03:15 世界医疗科技资讯

    

     绿茶因其强大的抗氧化功能而具有很多健康益处，但是一项针对炎症性肠病(inflammatory bowel disease, IBD)模式小鼠的新研究提示着同时摄入绿茶与膳食铁可能实际上降低绿茶的益处。相关研究结果于2016年3月8日在线发表在American Journal of Pathology期刊上，论文标题为“Epigallocatechin-3-Gallate Inhibition of Myeloperoxidase and Its Counter-Regulation by Dietary Iron and Lipocalin 2 in Murine Model of Gut Inflammation”。

     论文通信作者、美国宾夕法尼亚州立大学营养科学系助理教授Matam Vijay-Kumar说，“如果你在吃了富含铁的膳食后喝绿茶，那么绿茶中的一种主要化合物将与铁结合在一起。当这发生时，绿茶就丧失了作为一种抗氧化剂的潜力。为了获得绿茶的益处，可能最好还是不要在吃了富含铁的食物后喝它。” 富含铁的食物包括红色肉类和深色绿叶蔬菜，如甘蓝菜和菠菜。根据Vijay-Kumar的说法，同样的结果也适合于铁补充剂。

     在这项研究中，Vijay-Kumar和同事们发现，表没食子儿茶素没食子酸酯(EGCG)---绿茶中的一种主要化合物---强效地抑制炎症发生期间白细胞释放的一种被称作髓过氧化物酶(myeloperoxidase)的促炎性酶。利用EGCG让髓过氧化物酶失活可能也有助于缓解炎症性肠病(IBD)中的炎症。但是当同时摄入EGCG和铁时，与铁结合后，EGCG丧失了它的抑制髓过氧化物酶的能力。

     让事情更加复杂的是，研究人员还发现一种被称作脂质运载蛋白(lipocalin)的宿主蛋白也能够让EGCG失活，其中在炎症性疾病中，该蛋白大量存在。

     IBD的特征是消化道慢性炎症，这会导致出血性腹泻、疼痛、疲乏、体重降低和包括铁缺乏/贫血在内的其他症状。医生经常给IBD病人开铁补充剂药方。在这种情形下，同时摄入绿茶和铁补充剂可能帮倒忙，这是因为这两种营养物结合在一起而相互抵消。

     Vijay-Kumar说，“重要的是，摄入铁补充剂和绿茶的IBD病人应当知道一种营养物如何影响另一种营养物。这项研究的结果可能有助于因为绿茶的众多益处喜欢并且喝它的人，以及特地摄入绿茶治疗疾病的人。”

     论文第一作者、宾夕法尼亚州立大学营养科学系免疫学与传染病研究生Beng San Yeoh说，“绿茶的益处依赖于它的活性成分的生物利用度。它不仅是我们吃什么东西的问题，而且还是当我们吃时同时吃其他什么东西的问题。”

     原文阅读

     Epigallocatechin-3-Gallate Inhibition of Myeloperoxidase and Its Counter-Regulation by Dietary Iron and Lipocalin 2 in Murine Model of Gut Inflammation

     doi:10.1016/j.ajpath.2015.12.004

     Beng San Yeoh, Rodrigo Aguilera Olvera, Vishal Singh, Xia Xiao, Mary J. Kennett, Bina Joe, Joshua D. Lambert, Matam Vijay-Kumar

     Green tea-derived polyphenol (?)-epigallocatechin-3-gallate (EGCG) has been extensively studied for its antioxidant and anti-inflammatory properties in models of inflammatory bowel disease, yet the underlying molecular mechanism is not completely understood. Herein, we demonstrate that EGCG can potently inhibit the proinflammatory enzyme myeloperoxidase in vitro in a dose-dependent manner over a range of physiologic temperatures and pH values. The ability of EGCG to mediate its inhibitory activity is counter-regulated by the presence of iron and lipocalin 2. Spectral analysis indicated that EGCG prevents the peroxidase-catalyzed reaction by reverting the reactive peroxidase heme (compound I:oxoiron) back to its native inactive ferric state, possibly via the exchange of electrons. Further, administration of EGCG to dextran sodium sulfate–induced colitic mice significantly reduced the colonic myeloperoxidase activity and alleviated proinflammatory mediators associated with gut inflammation. However, the efficacy of EGCG against gut inflammation is diminished when orally coadministered with iron. These findings indicate that the ability of EGCG to inhibit myeloperoxidase activity is one of the mechanisms by which it exerts mucoprotective effects and that counter-regulatory factors such as dietary iron and luminal lipocalin 2 should be taken into consideration for optimizing clinical management strategies for inflammatory bowel disease with the use of EGCG treatment.

    

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