我们之前证明，甘草甜素 (GL) 可抑制氧化偶氮甲烷 (AOM)/葡聚糖硫酸钠 (DSS) 诱导的结直肠癌 (CC) 小鼠模型中的炎症和致癌作用。在这项研究中，我们发现模型小鼠的脾脏中存在调节性 T 细胞 (Treg) 的积累，并受到 GL 的抑制。 ICR小鼠被分为四组：对照、GL、CC和GL处理的CC（CC GL），并在AOM/DSS处理后20周处死。我们测量了脾脏重量、白髓和红髓面积、脾组织中的 CD8 T 细胞（细胞毒性 T 淋巴细胞，CTL）和 CD11c 阳性细胞（树突状细胞）以及叉头盒蛋白 3 (FoxP3) 阳性细胞 (Treg)在结直肠和脾组织中。在所有情况下，与对照组相比，CC 组均显示出显着增加，而 GL 给药显着减弱了这种增加。这些结果表明，脾脏中积累的Tregs可能通过抑制CTL参与炎症相关的癌发生。我们还认为，GL 与高迁移率族蛋白 1 (HMGB1) 结合，通过减少脾脏中的 Tregs 来抑制癌发生。此外，癌细胞中也有FoxP3的表达，表明其可能参与癌细胞的恶性转化。版权所有：©2024 Wang et al.这是一篇根据知识共享署名许可条款分发的开放获取文章，允许在任何媒体上不受限制地使用、分发和复制，前提是注明原始作者和来源。

We previously demonstrated that glycyrrhizin (GL) suppressed inflammation and carcinogenesis in an azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced murine model of colorectal cancer (CC). In this study, we found an accumulation of regulatory T cells (Tregs) in the spleen and suppression by GL in model mice. ICR mice were divided into four groups: Control, GL, CC, and GL-treated CC (CC+GL), and were sacrificed 20 weeks after AOM/DSS treatment. We measured spleen weight, areas of white and red pulp, and CD8+ T cells (cytotoxic T lymphocytes, CTL), and CD11c-positive cells (dendritic cells) in splenic tissues and forkhead box protein 3 (FoxP3)-positive cells (Tregs) in colorectal and splenic tissues. In all cases, the CC group showed a significant increase compared with those in Control group, and GL administration significantly attenuated this increase. These results indicate that Tregs accumulated in the spleen may participate in inflammation-related carcinogenesis by suppressing CTL. We also suggest that GL which binds to high-mobility group box 1 (HMGB1), suppresses carcinogenesis with decreasing Tregs in the spleen. Furthermore, there was an expression of FoxP3 in cancer cells, indicating that it may be involved in the malignant transformation of cancer cells.Copyright: © 2024 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.