Curcumin may impair iron status when fed to mice for six months.
Curcumin may impair iron status when fed to mice for six months.
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DOI：
10.1016/j.redox.2014.01.018
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发表时间：
2014
期刊：
影响因子：
11.4
通讯作者：
Pallauf K
中科院分区：
文献类型：
--
作者：
Chin D;Huebbe P;Frank J;Rimbach G;Pallauf K
姜黄素已被证明具有许多潜在的健康有益特性，在体外和动物模型中，姜黄素毒性的临床研究报告没有重大副作用。然而，姜黄素可能螯合膳食微量元素，因此可能产生潜在的不良影响。在这里，我们研究了6个月的饮食补充0.2%姜黄素对C57 BL/6 J小鼠铁，锌和铜状态的影响。与未补充的对照小鼠相比，我们观察到肝脏和脾脏中的铁储存显著减少，但锌和铜储存没有减少，并且在补充姜黄素的小鼠中强烈抑制了肝脏铁调素和铁蛋白表达。诱导铁输入转运蛋白二价金属转运蛋白1和转铁蛋白受体1的表达，而在姜黄素喂养的小鼠中，肝脏和脾脏炎症标志物不受影响。姜黄素的其他假定靶基因的mRNA表达，包括核因子（红细胞衍生2）样2和血红素加氧酶1在各组之间没有差异。大多数已发表的喂食姜黄素的动物试验都没有报道对铁状态或脾脏的不良影响。然而，长期补充姜黄素和西式饮食可能会加剧缺铁。因此，我们的研究结果表明，需要进一步的研究来评估姜黄素补充剂对铁状态的影响。在C57 BL/6 J小鼠中用0.2%姜黄素进行6个月的膳食补充导致肝脏和脾脏中的铁而不是锌和铜储存的显著减少，并且抑制肝脏铁调素和铁蛋白表达。此外，在姜黄素喂养的小鼠中诱导铁输入转运蛋白二价金属转运蛋白（DMT）1和转铁蛋白受体（TfR）1的表达。这些数据表明，长期补充姜黄素和西式饮食可能会加剧缺铁。0.2%姜黄素饮食6个月减少小鼠肝脏和脾脏中的铁储存。姜黄素在体内螯合铁，但不螯合锌和铜。姜黄素喂养的小鼠肝脏铁调素和铁蛋白的表达受到强烈抑制。姜黄素诱导肝脏铁转运蛋白DMT 1和TfR 1的表达。姜黄素不影响肝脏和脾脏的炎症和氧化标志物。
Curcumin has been shown to have many potentially health beneficial properties in vitro and in animal models with clinical studies on the toxicity of curcumin reporting no major side effects. However, curcumin may chelate dietary trace elements and could thus potentially exert adverse effects. Here, we investigated the effects of a 6 month dietary supplementation with 0.2% curcumin on iron, zinc, and copper status in C57BL/6J mice. Compared to non-supplemented control mice, we observed a significant reduction in iron, but not zinc and copper stores, in the liver and the spleen, as well as strongly suppressed liver hepcidin and ferritin expression in the curcumin-supplemented mice. The expression of the iron-importing transport proteins divalent metal transporter 1 and transferrin receptor 1 was induced, while hepatic and splenic inflammatory markers were not affected in the curcumin-fed mice. The mRNA expression of other putative target genes of curcumin, including the nuclear factor (erythroid-derived 2)-like 2 and haem oxygenase 1 did not differ between the groups. Most of the published animal trials with curcumin-feeding have not reported adverse effects on iron status or the spleen. However, it is possible that long-term curcumin supplementation and a Western-type diet may aggravate iron deficiency. Therefore, our findings show that further studies are needed to evaluate the effect of curcumin supplementation on iron status. A 6 month dietary supplementation with 0.2% curcumin in C57BL/6J mice led to a significant reduction in iron, but not zinc and copper stores, in the liver and the spleen, and suppressed liver hepcidin and ferritin expression. Furthermore, the expression of the iron-importing transport proteins divalent metal transporter (DMT) 1 and transferrin receptor (TfR) 1 was induced in the curcumin-fed mice. These data suggest that long-term curcumin supplementation and a Western-type diet may aggravate iron deficiency. 0.2% dietary curcumin for 6 months reduced iron stores in murine liver and spleen. Curcumin chelated iron but not zinc and copper in vivo. Liver hepcidin and ferritin expression was strongly suppressed in curcumin-fed mice. Curcumin induced expression of hepatic iron transporters DMT1 and TfR1. Curcumin did not affect hepatic and splenic inflammatory and oxidative markers.
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