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全β-葡聚糖颗粒减轻AOM/DSS诱导的小鼠结直肠癌发生——抑制肠道炎症。

Whole β-glucan particle attenuates AOM/DSS-induced colorectal tumorigenesis in mice inhibition of intestinal inflammation.

作者信息

Xie Yewen, Shao Fang, Duan Xuehan, Ding Jun, Ning Yongling, Sun Xiao, Xia Lei, Pan Jie, Chen Jie, He Shuyan, Shen Dong, Qi Chunjian

机构信息

Medical Research Center, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou, China.

Oncology Institute, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou, China.

出版信息

Front Pharmacol. 2023 Jan 12;14:1017475. doi: 10.3389/fphar.2023.1017475. eCollection 2023.

Abstract

Yeast β-glucan is a polysaccharide purified from cell wall, and its multiple biological activities are essential for immune regulation. However, the effect of β-glucan on the intestinal immune response during colitis-associated colorectal cancer (CAC) is unclear. Here, we explore the possible role of β-glucan in the development of CAC. Wild type (WT) mice with CAC induced by azoxmethane (AOM) and dextran sodium sulfate (DSS) had fewer tumors than untreated mice after oral β-glucan because of increased antitumor dendritic cells (DCs) in the tumor microenvironment, resulting in more CD8 T cells and the production of related cytokines. β-glucan also increased resistance to DSS-induced chronic colitis by reshaping the inflammatory microenvironment. These data suggest that β-glucan improves experimental intestinal inflammation and delays the development of CAC. Therefore, β-glucan is feasible for treating chronic colitis and CAC in clinical practice.

摘要

酵母β-葡聚糖是一种从细胞壁中纯化得到的多糖,其多种生物学活性对免疫调节至关重要。然而,β-葡聚糖在结肠炎相关结直肠癌(CAC)期间对肠道免疫反应的影响尚不清楚。在此,我们探讨β-葡聚糖在CAC发生发展中的可能作用。用偶氮甲烷(AOM)和葡聚糖硫酸钠(DSS)诱导产生CAC的野生型(WT)小鼠,口服β-葡聚糖后,由于肿瘤微环境中抗肿瘤树突状细胞(DCs)增多,导致更多的CD8 T细胞及相关细胞因子产生,其肿瘤数量比未处理小鼠少。β-葡聚糖还通过重塑炎症微环境增强了对DSS诱导的慢性结肠炎的抵抗力。这些数据表明,β-葡聚糖可改善实验性肠道炎症并延缓CAC的发展。因此,β-葡聚糖在临床实践中治疗慢性结肠炎和CAC是可行的。

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