富含美拉德反应产物的食物可抑制细胞增殖并诱导细胞死亡

B. Bartling, Grit Rehbein, V. Somoza, R. Silber, A. Simm
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引用次数: 8

摘要

美拉德反应产物(MRPs)和晚期糖基化终产物(AGEs)分别对应于热处理食品和体内氨基酸和还原糖之间的非酶糖基化最初产生的修饰蛋白衍生物。由于肺组织高度表达晚期糖基化终产物受体(RAGE),我们研究了富含MRP/ age的食物如面包皮(BC)和咖啡提取物(CE)对肺上皮(H358)细胞增殖和细胞死亡诱导的影响。在这里,我们发现CE对H358细胞增殖和活力的损害程度远高于BC。通过观察半胱天冬酶激活、磷脂酰丝氨酸暴露、外膜渗漏、线粒体功能障碍和应激激酶激活,CE诱导的细胞死亡表现出从凋亡到坏死的浓度依赖性转变。此外,高剂量CE触发活性氧的产生,从而介导caspase的抑制。两种食物的无毒浓度只会损害与细胞周期S/G2期细胞数量增加相关的增殖,而这与RAGE的过度表达无关。根据我们的数据,我们得出结论,富含MRP/ age的食物在中等浓度下介导抗增殖作用,这可能在癌症预防等生理条件下很重要,但在体外则会导致更高水平的细胞死亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Maillard reaction product‐rich food impair cell proliferation and induce cell death in vitro
Maillard reaction products (MRPs) and advanced glycation end-products (AGEs) correspond to modified protein derivatives that are initially generated by non-enzymatic glycation between amino acids and reducing sugars in heat-treated foods and in vivo, respectively. Because lung tissue highly expresses the receptor for advanced glycation end-products (RAGE), we studied the impact of MRP/AGE-rich foods like bread crust (BC) and coffee extract (CE) on the proliferation and cell death induction using lung epithelial (H358) cells. Here, we showed that CE impairs the proliferation and viability of H358 cells at much higher extent than BC does. Particularly cell death induced by CE showed a concentration-dependent shift from apoptotic to necrotic features as estimated by caspase activation, phosphatidylserine exposure, leakage of the outer membrane, mitochondrial dysfunction and stress kinase activation. Moreover, CE at higher dose triggered the generation of reactive oxygen species thereby mediating caspase inhibition. Non-toxic concentrations of both foods only impaired the proliferation associated with an increased amount of cells in the S/G2 phase of the cell cycle, which did not depend on the over-expression of RAGE. From our data we conclude that MRP/AGE-rich foods mediate antiproliferative effects at moderate concentrations that might be important in physiological conditions like cancer prevention but contributes to cell death at higher levels in vitro.
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