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 H2O2-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，硫酸化青钱柳多糖（SCP3）可以通过提高肠道的抗氧化能力来减轻肠道氧化应激（OS）损伤，但其机制仍需进一步探索。本研究旨在基于转录组分析揭示SCP3对肠上皮细胞（IEC-6）OS损伤的潜在保护机制。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H2O2诱导的IEC-6细胞的高凋亡率和线粒体膜电位降低。RNA测序结果显示,对照组和SCP3组有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。总之,SCP3通过抑制OS改善肠细胞损伤，可能与PI3K/Akt和MAPK信号通路密切相关。实际应用:本研究为青钱柳多糖作为抗氧化成分在辅助药物和功能食品中的实际应用提供了理论依据。
