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无机硒与水溶性且不可消化的山药多糖的共价接枝对丙烯酰胺损伤的IEC-6细胞具有更强的保护作用。

Covalent Grafting of Inorganic Selenium to the Water-Soluble and Nondigestive Chinese Yam Polysaccharides Causes Greater Protection of IEC-6 Cells with Acrylamide Injury.

作者信息

Wang Zhen-Xing, Zhang Li-Li, Zhao Xin-Huai

机构信息

Key Laboratory of Dairy Science, Ministry of Education, Northeast Agricultural University, Harbin 150030, China.

School of Biology and Food Engineering, Guangdong University of Petrochemical Technology, Maoming 525000, China.

出版信息

Foods. 2025 Apr 29;14(9):1560. doi: 10.3390/foods14091560.

DOI:10.3390/foods14091560
PMID:40361642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12071942/
Abstract

Acrylamide, a harmful substance generated during the normal thermal treatment of foods, has been shown to adversely affect human health, particularly the vital intestinal barrier function. Meanwhile, natural polysaccharides are recognized to exert an important biofunction in the intestine by protecting barrier integrity. In this study, the non-starch, water-soluble, and nondigestive yam polysaccharide (YP) was extracted from fresh Chinese yam, while two selenylated derivatives with different extents of selenylation were prepared via the HNO-NaSeO reaction system, and designated as YPSe-I and YPSe-II, respectively. Their protective activities and the associated molecular mechanisms of these substances against acrylamide-induced damage in rat intestinal epithelial (IEC-6) cells were thereby investigated. The experimental results demonstrated that the selenium contents of YPSe-I and YPSe-II were 0.80 and 1.48 g/kg, respectively, whereas that of the original YP was merely 0.04 g/kg. In IEC-6 cells, in comparison with YP, both YPSe-I and YPSe-II showed higher efficacy than YP in alleviating acrylamide-induced cell toxicity through promoting cell viability, suppressing the release of lactate dehydrogenase, and decreasing the generation of intracellular reactive oxygen species. Both YPSe-I and YPSe-II could also manifest higher effectiveness than YP in maintaining cell barrier integrity against the acrylamide-induced barrier disruption. The mentioned barrier protection was achieved by increasing transepithelial electrical resistance, reducing paracellular permeability, facilitating the distribution and expression of F-actin between the cells, and up-regulating the production of three tight junctions, namely ZO-1, occludin, and claudin-1. Additionally, acrylamide was observed to trigger the activation of the MAPK signaling pathway, thereby leading to cell barrier dysfunction. In contrast, YPSe-I and particularly YPSe-II were capable of down-regulating two MAPK-related proteins, namely p-p38 and p-JNK, and thereby inhibiting the acrylamide-induced activation of the MAPK signaling pathway. Moreover, YPSe-II in the cells was consistently shown to provide greater barrier protection than YPSe-I. In conclusion, chemical selenylation of YP could cause higher activity in mitigating acrylamide-induced cytotoxicity and intestinal barrier dysfunction, while the efficacy of activity enhancement was positively affected by the selenylation extent.

摘要

丙烯酰胺是食品正常热处理过程中产生的一种有害物质,已被证明会对人体健康产生不利影响,尤其是对重要的肠道屏障功能。同时,天然多糖被认为通过保护屏障完整性在肠道中发挥重要的生物功能。在本研究中,从新鲜山药中提取了非淀粉、水溶性且不可消化的山药多糖(YP),并通过HNO-NaSeO反应体系制备了两种不同硒化程度的硒化衍生物,分别命名为YPSe-I和YPSe-II。从而研究了这些物质对丙烯酰胺诱导的大鼠肠上皮(IEC-6)细胞损伤的保护活性及相关分子机制。实验结果表明,YPSe-I和YPSe-II的硒含量分别为0.80和1.48 g/kg,而原始YP的硒含量仅为0.04 g/kg。在IEC-6细胞中,与YP相比,YPSe-I和YPSe-II在减轻丙烯酰胺诱导的细胞毒性方面均表现出比YP更高的功效,具体表现为促进细胞活力、抑制乳酸脱氢酶释放以及减少细胞内活性氧的产生。YPSe-I和YPSe-II在维持细胞屏障完整性以抵抗丙烯酰胺诱导的屏障破坏方面也比YP表现出更高的有效性。上述屏障保护是通过增加跨上皮电阻、降低细胞旁通透性、促进细胞间F-肌动蛋白的分布和表达以及上调三种紧密连接蛋白(即ZO-1、闭合蛋白和Claudin-1)的产生来实现的。此外,观察到丙烯酰胺会触发丝裂原活化蛋白激酶(MAPK)信号通路的激活,从而导致细胞屏障功能障碍。相比之下,YPSe-I尤其是YPSe-II能够下调两种与MAPK相关的蛋白,即p-p38和p-JNK,从而抑制丙烯酰胺诱导的MAPK信号通路激活。此外,细胞中的YPSe-II始终显示出比YPSe-I提供更强的屏障保护作用。总之,YP的化学硒化在减轻丙烯酰胺诱导的细胞毒性和肠道屏障功能障碍方面具有更高的活性,而活性增强的效果受到硒化程度的正向影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/beb29d61c390/foods-14-01560-g009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/553338d44f26/foods-14-01560-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/04378d0f5acd/foods-14-01560-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/a9157f0dfe8a/foods-14-01560-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/beb29d61c390/foods-14-01560-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/6fa4f52ea1f8/foods-14-01560-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/99f810ae35ed/foods-14-01560-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/b6b881894b86/foods-14-01560-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/6177e5b9b99e/foods-14-01560-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/553338d44f26/foods-14-01560-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/2a3243ad56c4/foods-14-01560-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/04378d0f5acd/foods-14-01560-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/a9157f0dfe8a/foods-14-01560-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c22b/12071942/beb29d61c390/foods-14-01560-g009.jpg

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