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转录组谱分析揭示了环磷腺苷葡甲胺对 IEC-6 细胞氧化损伤的保护机制。

Transcriptome profiling reveals the protective mechanism of sulfated Cyclocarya paliurus polysaccharides against oxidative damage of IEC-6 cell.

机构信息

State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang, Jiangxi, China.

Department of Biology and Food Engineering, Bozhou University, Bozhou, Anhui, China.

出版信息

J Food Sci. 2024 Sep;89(9):5858-5869. doi: 10.1111/1750-3841.17173. Epub 2024 Jul 23.

DOI:10.1111/1750-3841.17173
PMID:39042473
Abstract

Our previous studies have shown that sulfated Cyclocarya paliurus polysaccharides (SCP3) can alleviate intestinal oxidative stress (OS) damage by improving the antioxidant capacity of the intestine, but its mechanism still needs further exploration. This study aimed to reveal the possible underlying protective mechanism of SCP3 against OS damage of intestinal epithelial cells (IEC-6) based on transcriptome profiling. The results showed that SCP3 could increase the activity of superoxide dismutase and reduce the production of malondialdehyde and reactive oxygen species. In addition, the SCP3 could also alleviate the HO-induced high apoptosis rate and mitochondrial membrane potential decrease in IEC-6 cells. RNA-sequencing results showed that there were 2152 differentially expressed genes between the control group and the SCP3 group, and the mitogen-activated protein kinases (MAPK) and PI3K-Akt signaling pathways are the main signaling pathways that contributed to SCP3 protecting IEC-6 cells from OS damage. In summary, the SCP3 plays a role in improving intestinal cell damage by inhibiting OS, which may be closely related to the PI3K/Akt and MAPK signaling pathways. PRACTICAL APPLICATION: This study provides a theoretical basis for the practical application of Cyclocarya paliurus polysaccharides as an antioxidant ingredient in auxiliary medicines and functional foods.

摘要

我们之前的研究表明,环磷腺苷葡甲胺(SCP3)可以通过提高肠道抗氧化能力来减轻肠道氧化应激(OS)损伤,但它的机制仍需要进一步探索。本研究旨在基于转录组谱分析揭示 SCP3 对肠上皮细胞(IEC-6)OS 损伤的可能潜在保护机制。结果表明,SCP3 可以提高超氧化物歧化酶的活性,减少丙二醛和活性氧的产生。此外,SCP3 还可以减轻 HO 诱导的 IEC-6 细胞高凋亡率和线粒体膜电位降低。RNA-seq 结果显示,对照组和 SCP3 组之间有 2152 个差异表达基因,丝裂原活化蛋白激酶(MAPK)和 PI3K-Akt 信号通路是 SCP3 保护 IEC-6 细胞免受 OS 损伤的主要信号通路。综上所述,SCP3 通过抑制 OS 发挥改善肠道细胞损伤的作用,这可能与 PI3K/Akt 和 MAPK 信号通路密切相关。

实际应用

本研究为将环磷腺苷葡甲胺作为辅助药物和功能性食品中的抗氧化成分的实际应用提供了理论依据。

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